Travma 2012-5

Page 1



Cilt - Volume 18

Sayı - Number 5

Eylül - September 2012

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY

www.tjtes.org Index Medicus, Medline, EMBASE/Excerpta Medica, Science Citation Index-Expanded (SCI-E), Index Copernicus ve TÜB‹TAK-ULAKB‹M Türk Tıp Dizini’nde yer almaktadır. Indexed in Index Medicus, Medline, EMBASE/Excerpta Medica and Science Citation Index-Expanded (SCI-E), Index Copernicus and the Turkish Medical Index of TÜB‹TAK-ULAKB‹M.

ISSN 1306 - 696x



ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ TURKISH JOURNAL OF TRAUMA AND EMERGENCY SURGERY Editör (Editor) Recep Güloğlu Yardımcı Editörler (Associate Editors) Kaya Sarıbeyoğlu Hakan Yanar Ahmet Nuray Turhan Geçmiş Dönem Editörleri (Former Editors) Ömer Türel Cemalettin Ertekin Korhan Taviloğlu

ULUSAL BİLİMSEL DANIŞMA KURULU (NATIONAL EDITORIAL BOARD) Fatih Ağalar Yılmaz Akgün Levhi Akın Alper Akınoğlu Murat Aksoy Şeref Aktaş Ali Akyüz Ömer Alabaz Nevzat Alkan Edit Altınlı Acar Aren Gamze Aren Cumhur Arıcı Oktar Asoğlu Ali Atan Bülent Atilla Levent Avtan Yunus Aydın Önder Aydıngöz Erşan Aygün Mois Bahar Akın Eraslan Balcı Emre Balık Umut Barbaros Semih Baskan M Murad Başar Mehmet Bayramiçli Ahmet Bekar Orhan Bilge Mustafa Bozbuğa Mehmet Can Başar Cander Nuh Zafer Cantürk Münacettin Ceviz Banu Coşar Figen Coşkun İrfan Coşkun Nahit Çakar Adnan Çalık Fehmi Çelebi Gürhan Çelik Oğuz Çetinkale M. Ercan Çetinus Sebahattin Çobanoğlu Ahmet Çoker Cemil Dalay Fatih Dikici Yalım Dikmen Osman Nuri Dilek Kemal Dolay Levent Döşemeci Murat Servan Döşoğlu Kemal Durak Engin Dursun Atilla Elhan

İstanbul Çanakkale İstanbul Adana İstanbul İstanbul İstanbul Adana İstanbul İstanbul İstanbul İstanbul Antalya İstanbul Ankara Ankara İstanbul İstanbul İstanbul İstanbul İstanbul Elazığ İstanbul İstanbul Ankara Kırıkkale İstanbul Bursa İstanbul Edirne İstanbul Konya Kocaeli Erzurum İstanbul Ankara Edirne İstanbul Trabzon Erzurum İstanbul İstanbul İstanbul Edirne İzmir Adana İstanbul İstanbul Sakarya Antalya Antalya Düzce Bursa Ankara Ankara

Mehmet Eliçevik İmdat Elmas Ufuk Emekli Haluk Emir Yeşim Erbil Şevval Eren Hayri Erkol Metin Ertem Mehmet Eryılmaz Figen Esen Tarık Esen İrfan Esenkaya Ozlem Evren Kemer Nurperi Gazioğlu Fatih Ata Genç Alper Gökçe Niyazi Görmüş Feryal Gün Ömer Günal Nurullah Günay Haldun Gündoğdu Mahir Günşen Emin Gürleyik Hakan Güven İbrahim İkizceli Haluk İnce Fuat İpekçi Ferda Şöhret Kahveci Selin Kapan Murat Kara Hasan Eşref Karabulut Ekrem Kaya Mehmet Yaşar Kaynar Mete Nur Kesim Yusuf Alper Kılıç Haluk Kiper Hikmet Koçak M Hakan Korkmaz Güniz Meyancı Köksal Cüneyt Köksoy İsmail Kuran Necmi Kurt Mehmet Kurtoğlu Nezihi Küçükarslan İsmail Mihmanlı Mehmet Mihmanlı Köksal Öner Durkaya Ören Hüseyin Öz Hüseyin Özbey Faruk Özcan Cemal Özçelik İlgin Özden Mehmet Özdoğan Şükrü Özer

İstanbul İstanbul İstanbul İstanbul İstanbul Diyarbakır Bolu İstanbul Ankara İstanbul İstanbul Malatya Ankara İstanbul İstanbul Tekirdağ Konya İstanbul Düzce Kayseri Ankara Adana Bolu İstanbul İstanbul İstanbul İzmir Bursa İstanbul Ankara İstanbul Bursa İstanbul Samsun Ankara Eskişehir Erzurum Ankara İstanbul Ankara İstanbul İstanbul İstanbul Ankara İstanbul İstanbul İstanbul Erzurum İstanbul İstanbul İstanbul Diyarbakır İstanbul Ankara Konya

Halil Özgüç Ahmet Özkara Mahir Özmen Vahit Özmen Volkan Öztuna Niyazi Özüçelik Süleyman Özyalçın Emine Özyuvacı Salih Pekmezci İzzet Rozanes Kazım Sarı Esra Can Say Ali Savaş İskender Sayek Tülay Özkan Seyhan Gürsel Remzi Soybir Yunus Söylet Erdoğan Sözüer Mustafa Şahin Cüneyt Şar Mert Şentürk Feridun Şirin İbrahim Taçyıldız Gül Köknel Talu Ertan Tatlıcıoğlu Gonca Tekant Cihangir Tetik Mustafa Tireli Alper Toker Rıfat Tokyay Salih Topçu Turgut Tufan Fatih Tunca Akif Turna Zafer Nahit Utkan Ali Uzunköy Erol Erden Ünlüer Özgür Yağmur Müslime Yalaz Serhat Yalçın Sümer Yamaner Mustafa Yandı Nihat Yavuz Cumhur Yeğen Ebru Yeşildağ Hüseyin Yetik Cuma Yıldırım Bedrettin Yıldızeli Sezai Yılmaz Kaya Yorgancı Coşkun Yorulmaz Tayfun Yücel

Bursa İstanbul Ankara İstanbul Mersin İstanbul İstanbul İstanbul İstanbul İstanbul İstanbul İstanbul Ankara Ankara İstanbul Tekirdağ İstanbul Kayseri Tokat İstanbul İstanbul İstanbul Diyarbakır İstanbul Ankara İstanbul İstanbul Manisa İstanbul İstanbul Kocaeli Ankara İstanbul İstanbul Kocaeli Urfa İzmir Adana İstanbul İstanbul İstanbul Trabzon İstanbul İstanbul Tekirdağ İstanbul Gaziantep İstanbul Malatya Ankara İstanbul İstanbul


ULUSLARARASI BİLİMSEL DANIŞMA KURULU INTERNATIONAL EDITORIAL BOARD

Juan Asensio Zsolt Balogh Ken Boffard Fausto Catena Howard Champion Elias Degiannis Demetrios Demetriades Timothy Fabian Rafi Gürünlüoğlu Clem W. Imrie Kenji Inaba Rao Ivatury Yoram Kluger Rifat Latifi Sten Lennquist Ari Leppaniemi Valerie Malka Ingo Marzi Kenneth L. Mattox Carlos Mesquita

Miami, USA New Castle, Australia Johannesburg, S. Africa Bologna, Italy Washington DC, USA Johannesburg, S. Africa Los Angeles, USA Memphis, USA Denver, USA Glasgow, Scotland Los Angeles, USA Richmond, USA Haifa, Israel Tucson, USA Malmö, Sweden Helsinki, Finland Sydney, Australia Frankfurt, Germany Houston, USA Coimbra, Portugal

Ernest E Moore Pradeep Navsaria Andrew Nicol Hans J Oestern Andrew Peitzman Basil A Pruitt Peter Rhee Pol Rommens William Schwabb Michael Stein Spiros Stergiopoulos Michael Sugrue Otmar Trentz Donald Trunkey Fernando Turegano Selman Uranues Vilmos Vecsei George Velmahos Eric J Voiglio Mauro Zago

Denver, USA Cape Town, S. Africa Cape Town, S. Africa Celle, Germany Pittsburgh, USA San Antonio, USA Tucson, USA Mainz, Germany Philadelphia, USA Petach-Tikva, Israel Athens, Greece Liverpool, Australia Zurich, Switzerland Oregon, USA Madrid, Spain Graz, Austria Vienna, Austria Boston, USA Lyon, France Milan, Italy

REDAKSİYON (REDACTION) Erman Aytaç

ULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERY

Başkan (President) Başkan Yardımcısı (Vice President) Genel Sekreter (Secretary General) Sayman (Treasurer) Yönetim Kurulu Üyeleri (Members)

Recep Güloğlu Kaya Sarıbeyoğlu Ahmet Nuray Turhan Hakan Yanar M. Mahir Özmen Ediz Altınlı Gürhan Çelik

İLETİŞİM (CORRESPONDENCE)

Ulusal Travma ve Acil Cerrahi Derneği Şehremini Mah., Köprülü Mehmet Paşa Sok. Dadaşoğlu Apt., No: 25/1, 34104 Şehremini, İstanbul

Tel: +90 212 - 588 62 46 - 588 62 46 Faks (Fax): +90 212 - 586 18 04 e-posta (e-mail): travma@travma.org.tr Web: www.travma.org.tr

ULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ YAYIN ORGANI ISSUED BY THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERY

Ulusal Travma ve Acil Cerrahi Derneği adına Sahibi (Owner) Yazı İşleri Müdürü (Editorial Director) Yayın Koordinatörü (Managing Editor) Amblem Yazışma adresi (Correspondence address) Tel Faks (Fax)

Recep Güloğlu Recep Güloğlu M. Mahir Özmen Metin Ertem Ulusal Travma ve Acil Cerrahi Dergisi Sekreterliği Şehremini Mah., Köprülü Mehmet Paşa Sok., Dadaşoğlu Apt., No: 25/1, 34104 Şehremini, İstanbul +90 212 - 531 12 46 - 588 62 46 +90 212 - 586 18 04

Abonelik: 2011 yılı abone bedeli (Ulusal Travma ve Acil Cerrahi Derneği’ne bağış olarak) 75.- YTL’dir. Hesap No: Türkiye İş Bankası, İstanbul Tıp Fakültesi Şubesi 1200 - 3141069 no’lu hesabına yatırılıp makbuz dernek adresine posta veya faks yolu ile iletilmelidir. Annual subscription rates: 75.- (USD) p-ISSN 1306-696x • e-ISSN 1307-7945 • Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus ve TÜBİTAK ULAKBİM Türk Tıp Dizini’nde yer almaktadır. (Included in Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus and Turkish Medical Index) • Yayıncı (Publisher): KARE Yayıncılık (karepublishing) • Tasarım (Design): Ali Cangül • İngilizce Editörü (Linguistic Editor): Corinne Can • İstatistik (Statistician): Empiar • Online Dergi & Web (Online Manuscript & Web Management): LookUs • Baskı (Press): Yıldırım Matbaacılık • Basım tarihi (Press date): Eylül (September) 2012 • Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur. (This publication is printed on paper that meets the international standard ISO 9706: 1994).


YAZARLARA BİLGİ Ulusal Travma ve Acil Cerrahi Dergisi, Ulusal Travma ve Acil Cerrahi Derneği’nin yayın organıdır. Travma ve acil cerrahi hastalıklar konularında bilimsel birikime katkısı olan klinik ve deneysel çalışmaları, editöryel yazıları, klinik olgu sunumlarını ve bu konulardaki teknik katkılar ile son gelişmeleri yayınlar. Dergi iki ayda bir yayınlanır. Ulusal Travma ve Acil Cerrahi Dergisi, 2001 yılından itibaren Index Medicus ve Medline’da, 2005 yılından itibaren Excerpta Medica / EMBASE indekslerinde, 2007 yılından itibaren Science Citation Index-Expanded (SCI-E) ile Journal Citation Reports / Science Edition uluslararası indekslerinde ve 2008 yılından itibaren Index Copernicus indeksinde yer almaktadır. 2001-2006 yılları arasındaki 5 yıllık dönemde SCI-E kapsamındaki dergilerdeki İmpakt faktörümüz 0,5 olmuştur. Dergide araştırma yazılarına öncelik verilmekte, bu nedenle derleme veya olgu sunumu türündeki yazılarda seçim ölçütleri daha dar tutulmaktadır. PUBMED’de dergi “Ulus Travma Acil Cerrahi Derg” kısaltması ile yer almaktadır. Dergiye yazı teslimi, çalışmanın daha önce yayınlanmadığı (özet ya da bir sunu, inceleme, ya da tezin bir parçası şeklinde yayınlanması dışında), başka bir yerde yayınlanmasının düşünülmediği ve Ulusal Travma ve Acil Cerrahi Dergisi’nde yayınlanmasının tüm yazarlar tarafından uygun bulunduğu anlamına gelmektedir. Yazar(lar), çalışmanın yayınlanmasının kabulünden başlayarak, yazıya ait her hakkı Ulusal Travma ve Acil Cerrahi Derneği’ne devretmektedir(ler). Yazar(lar), izin almaksızın çalışmayı başka bir dilde ya da yerde yayınlamayacaklarını kabul eder(ler). Gönderilen yazı daha önce herhangi bir toplantıda sunulmuş ise, toplantı adı, tarihi ve düzenlendiği şehir belirtilmelidir. Dergide Türkçe ve İngilizce yazılmış makaleler yayınlanabilir. Tüm yazılar önce editör tarafından ön değerlendirmeye alınır; daha sonra incelenmesi için danışma kurulu üyelerine gönderilir. Tüm yazılarda editöryel değerlendirme ve düzeltmeye başvurulur; gerektiğinde, yazarlardan bazı soruları yanıtlanması ve eksikleri tamamlanması istenebilir. Dergide yayınlanmasına karar verilen yazılar “manuscript editing” sürecine alınır; bu aşamada tüm bilgilerin doğruluğu için ayrıntılı kontrol ve denetimden geçirilir; yayın öncesi şekline getirilerek yazarların kontrolüne ve onayına sunulur. Editörün, kabul edilmeyen yazıların bütününü ya da bir bölümünü (tablo, resim, vs.) iade etme zorunluluğu yoktur. Yazıların hazırlanması: Tüm yazılı metinler 12 punto büyüklükte “Times New Roman” yazı karakterinde iki satır aralıklı olarak yazılmalıdır. Sayfada her iki tarafta uygun miktarda boşluk bırakılmalı ve ana metindeki sayfalar numaralandırılmalıdır. Journal Agent sisteminde, başvuru mektubu, başlık, yazarlar ve kurumları, iletişim adresi, Türkçe özet ve yazının İngilizce başlığı ve özeti ilgili aşamalarda yüklenecektir. İngilizce yazılan çalışmalara da Türkçe özet eklenmesi gerekmektedir. Yazının ana metnindeyse şu sıra kullanılacaktır: Giriş, Gereç ve Yöntem, Bulgular, Tartışma, Teşekkür, Kaynaklar, Tablolar ve Şekiller. Başvuru mektubu: Bu mektupta yazının tüm yazarlar tarafından okunduğu, onaylandığı ve orijinal bir çalışma ürünü olduğu ifade edilmeli ve yazar isimlerinin yanında imzaları bulunmalıdır. Başvuru mektubu ayrı bir dosya olarak, Journal Agent sisteminin “Yeni Makale Gönder” bölümünde, 10. aşamada yer alan dosya yükleme aşamasında yollanmalıdır. Başlık sayfası: Yazının başlığı, yazarların adı, soyadı ve ünvanları, çalışmanın yapıldığı kurumun adı ve şehri, eğer varsa çalışmayı destekleyen fon ve kuruluşların açık adları bu sayfada yer almalıdır. Bu sayfaya ayrıca “yazışmadan sorumlu” yazarın isim, açık adres, telefon, faks, mobil telefon ve e-posta bilgileri eklenmelidir. Özet: Çalışmanın gereç ve yöntemini ve bulgularını tanıtıcı olmalıdır. Türkçe özet, Amaç, Gereç ve Yöntem, Bulgular, Sonuç ve Anahtar Sözcükler başlıklarını; İngilizce özet Background, Methods, Results, Conclusion ve Key words başlıklarını içermelidir. İngilizce olarak hazırlanan çalışmalarda da Türkçe özet yer almalıdır. Özetler başlıklar hariç 190-210 sözcük olmalıdır. Tablo, şekil, grafik ve resimler: Şekillere ait numara ve açıklayıcı bilgiler ana metinde ilgili bölüme yazılmalıdır. Mikroskobik şekillerde resmi açıklayıcı bilgilere ek olarak, büyütme oranı ve kullanılan boyama tekniği de belirtilmelidir. Yazarlara ait olmayan, başka kaynaklarca daha önce yayınlanmış tüm resim, şekil ve tablolar için yayın hakkına sahip kişiler-

den izin alınmalı ve izin belgesi dergi editörlüğüne ayrıca açıklamasıyla birlikte gönderilmelidir. Hastaların görüntülendiği fotoğraflara, hastanın ve/veya velisinin imzaladığı bir izin belgesi eşlik etmeli veya fotoğrafta hastanın yüzü tanınmayacak şekilde kapatılmış olmalıdır. Renkli resim ve şekillerin basımı için karar hakemler ve editöre aittir. Yazarlar renkli baskının hazırlık aşamasındaki tutarını ödemeyi kabul etmelidirler. Kaynaklar: Metin içindeki kullanım sırasına göre düzenlenmelidir. Makale içinde geçen kaynak numaraları köşeli parantezle ve küçültülmeden belirtilmelidir. Kaynak listesinde yalnızca yayınlanmış ya da yayınlanması kabul edilmiş çalışmalar yer almalıdır. Kaynak bildirme “Uniform Requirements for Manuscripts Submitted to Biomedical Journals” (http:// www.icmje.org) adlı kılavuzun en son güncellenmiş şekline (Şubat 2006) uymalıdır. Dergi adları Index Medicus’a uygun şekilde kısaltılmalıdır. Altı ya da daha az sayıda olduğunda tüm yazar adları verilmeli, daha çok yazar durumunda altıncı yazarın arkasından “et al.” ya da “ve ark.” eklenmelidir. Kaynakların dizilme şekli ve noktalamalar aşağıdaki örneklere uygun olmalıdır: Dergi metni için örnek: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5. Kitaptan bölüm için örnek: Jurkovich GJ. Duodenum and pancreas. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: McGraw-Hill; 2000. p. 735-62. Sizlerin çalışmalarınızda kaynak olarak yararlanabilmeniz için www.travma.org.tr adresli web sayfamızda eski yayınlara tam metin olarak ulaşabileceğiniz bir arama motoru vardır. Derleme yazıları: Bu tür makaleler editörler kurulu tarafından gerek olduğunda, konu hakkında birikimi olan ve bu birikimi literatüre de yansımış kişilerden talep edilecek ve dergi yazım kurallarına uygunluğu saptandıktan sonra değerlendirmeye alınacaktır. Derleme makaleleri; başlık, Türkçe özet, İngilizce başlık ve özet, alt başlıklarla bölümlendirilmiş metin ile kaynakları içermelidir. Tablo, şekil, grafik veya resim varsa yukarıda belirtildiği şekilde gönderilmelidir. Olgu sunumları: Derginin her sayısında sınırlı sayıda olgu sunumuna yer verilmektedir. Olgu bildirilerinin kabulünde, az görülürlük, eğitici olma, ilginç olma önemli ölçüt değerlerdir. Ayrıca bu tür yazıların olabildiğince kısa hazırlanması gerekir. Olgu sunumları başlık, Türkçe özet, İngilizce başlık ve özet, olgu sunumu, tartışma ve kaynaklar bölümlerinden oluşmalıdır. Bu tür çalışmalarda en fazla 5 yazara yer verilmesine özen gösterilmelidir. Editöre mektuplar: Editöre mektuplar basılı dergide ve PUBMED’de yer almamakta, ancak derginin web sitesinde yayınlanmaktadır. Bu mektuplar için dergi yönetimi tarafından yayın belgesi verilmemektedir. Daha önce basılmış yazılarla ilgili görüş, katkı, eleştiriler ya da farklı bir konu üzerindeki deneyim ve düşünceler için editöre mektup yazılabilir. Bu tür yazılar 500 sözcüğü geçmemeli ve tıbbi etik kurallara uygun olarak kaleme alınmış olmalıdır. Mektup basılmış bir yazı hakkında ise, söz konusu yayına ait yıl, sayı, sayfa numaraları, yazı başlığı ve yazarların adları belirtilmelidir. Mektup bir konuda deneyim, düşünce hakkında ise verilen bilgiler doğrultusunda dergi kurallarına uyumlu olarak kaynaklar da belirtilmelidir. Bilgilendirerek onay alma - Etik: Deneysel çalışmaların sonuçlarını bildiren yazılarda, çalışmanın yapıldığı gönüllü ya da hastalara uygulanacak prosedür(lerin) özelliği tümüyle anlatıldıktan sonra, onaylarının alındığını gösterir bir cümle bulunmalıdır. Yazarlar, bu tür bir çalışma söz konusu olduğunda, uluslararası alanda kabul edilen kılavuzlara ve T.C. Sağlık Bakanlığı tarafından getirilen yönetmelik ve yazılarda belirtilen hükümlere uyulduğunu belirtmeli ve kurumdan aldıkları Etik Komitesi onayını göndermelidir. Hayvanlar üzerinde yapılan çalışmalarda ağrı, acı ve rahatsızlık verilmemesi için neler yapıldığı açık bir şekilde belirtilmelidir. Yazı gönderme - Yazıların gönderilmesi: Ulusal Travma ve Acil Cerrahi Dergisi yalnızca www.travma.org.tr adresindeki internet sitesinden on-line olarak gönderilen yazıları kabul etmekte, posta yoluyla yollanan yazıları değerlendirmeye almamaktadır. Tüm yazılar ilgili adresteki “Online Makale Gönderme” ikonuna tıklandığında ulaşılan Journal Agent sisteminden yollanmaktadır. Sistem her aşamada kullanıcıyı bilgilendiren özelliktedir.


INFORMATION FOR THE AUTHORS The Turkish Journal of Trauma and Emergency Surgery (TJTES) is an official publication of the Turkish Association of Trauma and Emergency Surgery. It is a peer-reviewed periodical that considers for publication clinical and experimental studies, case reports, technical contributions, and letters to the editor. Six issues are published annually. As from 2001, the journal is indexed in Index Medicus and Medline, as from 2005 in Excerpta Medica and EMBASE, as from 2007 in Science Citation Index Expanded (SCI-E) and Journal Citation Reports / Science Edition, and as from 2008 in Index Copernicus. For the five-year term of 2001-2006, our impact factor in SCI-E indexed journals is 0.5. It is cited as ‘Ulus Travma Acil Cerrahi Derg’ in PUBMED. Submission of a manuscript by electronic means implies: that the work has not been published before (except in the form of an abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; and that its publication in the Turkish Journal of Trauma and Emergency Surgery is approved by all co-authors. The author(s) transfer(s) the copyright to the Turkish Association of Trauma and Emergency Surgery to be effective if and when the manuscript is accepted for publication. The author(s) guarantee(s) that the manuscript will not be published elsewhere in any other language without the consent of the Association. If the manuscript has been presented at a meeting, this should be stated together with the name of the meeting, date, and the place. Manuscripts may be submitted in Turkish or in English. All submissions are initially reviewed by the editor, and then are sent to reviewers. All manuscripts are subject to editing and, if necessary, will be returned to the authors for answered responses to outstanding questions or for addition of any missing information to be added. For accuracy and clarity, a detailed manuscript editing is undertaken for all manuscripts accepted for publication. Final galley proofs are sent to the authors for approval.

Abstract: The abstract should be structured and serve as an informative guide for the methods and results sections of the study. It must be prepared with the following subtitles: Background, Methods, Results and Conclusions. Abstracts should not exceed 200 words. Figures, illustrations and tables: All figures and tables should be numbered in the order of appearance in the text. The desired position of figures and tables should be indicated in the text. Legends should be included in the relevant part of the main text and those for photomicrographs and slide preparations should indicate the magnification and the stain used. Color pictures and figures will be published if they are definitely required and with the understanding that the authors are prepared to bear the costs. Line drawings should be professionally prepared. For recognizable photographs, signed releases of the patient or of his/her legal representatives should be enclosed; otherwise, patient names or eyes must be blocked out to prevent identification. References: All references should be numbered in the order of mention in the text. All reference figures in the text should be given in brackets without changing the font size. References should only include articles that have been published or accepted for publication. Reference format should conform to the “Uniform requirements for manuscripts submitted to biomedical journals” (http://www.icmje.org) and its updated versions (February 2006). Journal titles should be abbreviated according to Index Medicus. Journal references should provide inclusive page numbers. All authors, if six or fewer, should be listed; otherwise the first six should be listed, followed by “et al.” should be written. The style and punctuation of the references should follow the formats below: Journal article: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5.

Unless specifically indicated otherwise at the time of submission, rejected manuscripts will not be returned to the authors, including accompanying materials.

Chapter in book: Jurkovich GJ. Duodenum and pancreas. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: McGraw-Hill; 2000. p. 735-62.

TJTES is indexed in Science Citation Index-Expanded (SCI-E), Index Medicus, Medline, EMBASE, Excerpta Medica, and the Turkish Medical Index of TUBITAK-ULAKBIM. Priority of publications is given to original studies; therefore, selection criteria are more refined for reviews and case reports.

Our journal has succeeded in being included in several indexes, in this context, we have included a search engine in our web site (www. travma.org.tr) so that you can access full-text articles of the previous issues and cite the published articles in your studies.

Manuscript submission: TJTES accepts only on-line submission via the official web site (please click, www.travma.org.tr/en) and refuses printed manuscript submissions by mail. All submissions are made by the on-line submission system called Journal Agent, by clicking the icon “Online manuscript submission” at the above mentioned web site homepage. The system includes directions at each step but for further information you may visit the web site (http://www.travma.org/en/ journal/). Manuscript preparation: Manuscripts should have double-line spacing, leaving sufficient margin on both sides. The font size (12 points) and style (Times New Roman) of the main text should be uniformly taken into account. All pages of the main text should be numbered consecutively. Cover letter, manuscript title, author names and institutions and correspondence address, abstract in Turkish (for Turkish authors only), and title and abstract in English are uploaded to the Journal Agent system in the relevant steps. The main text includes Introduction, Materials and Methods, Results, Discussion, Acknowledgments, References, Tables and Figure Legends. The cover letter must contain a brief statement that the manuscript has been read and approved by all authors, that it has not been submitted to, or is not under consideration for publication in, another journal. It should contain the names and signatures of all authors. The cover letter is uploaded at the 10th step of the “Submit New Manuscript” section, called “Upload Your Files”.

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ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY C‹LT - VOL. 18

SAYI - NUMBER 5 EYLÜL - SEPTEMBER 2012

İçindekiler - Contents

Deneysel Çalışma - Experimental Study 367-375 The effect of catheter use on vein grafting of a peripheral nerve defect: an experimental study Ven grefti ile periferik sinir defektlerinin onarımında kateter kullanımının sinir rejenerasyonuna etkisi: Deneysel çalışma Bayraktar AM, Özbek S, Özcan M, Noyan B, Çavuşoğlu İ 376-383 Comparison of topical zinc oxide and silver sulfadiazine in burn wounds: an experimental study Yanık yarası tedavisinde topikal çinko oksit ile gümüş sülfadiazinin karşılaştırılması: Deneysel çalışma Arslan K, Karahan Ö, Okuş A, Ünlü Y, Eryılmaz MA, Ay S, Sevinç

Klinik Çalışma - Original Articles 384-388 The value of serum fibrinogen level in the diagnosis of acute appendicitis Akut apandisit tanısında serum fibrinojen düzeyinin değeri Menteş Ö, Eryılmaz M, Harlak A, Öztürk E, Tufan T 389-396 Incarcerated abdominal wall hernia surgery: relationship between risk factors and morbidity and mortality rates (a single center emergency surgery experience) Boğulmuş abdominal duvar herni cerrahisi: Morbidite ve mortalite insidansının risk faktörleriyle ilişkisinin analizi (Tek merkezli acil cerrahi deneyimi) Özkan E, Yıldız MK, Çakır T, Dulundu E, Eriş C, Fersahoğlu MM, Topaloğlu Ü 397-404 Randomized controlled trial of morphine in elderly patients with acute abdominal pain Akut karın ağrısı olan yaşlı hastalarda morfinin randomize kontrollü bir çalışması Güngör F, Kartal M, Bektaş F, Söyüncü S, Yiğit Ö, Mesci A 405-410 Treatment of acute and closed Achilles tendon ruptures by minimally invasive tenocutaneous suturing Minimal invaziv tenokutanöz dikişle akut ve kapalı Aşil tendonu yırtığının tedavisi Ding W, Yan W, Zhu Y, Liu Z 411-416 Çocuk ve erişkin minör kafa travmalarında kan S100B ile laktatın rolü ve bilgisayarlı beyin tomografisi ile korelasyonu The role of blood S100B and lactate levels in minor head traumas in children and adults and correlation with brain computerized tomography Sezer AA, Akıncı E, Öztürk M, Coşkun F, Yılmaz G, Karakaş A, Toksöz T 417-423 Erken fasyotominin yılan ısırıkları tedavisindeki etkinliği Effectiveness of early fasciotomy in the management of snakebites Fırat C, Erbatur S, Aytekin AH, Kılınç H 424-428 Temporal bone fractures: evaluation of 77 patients and a management algorithm Temporal kemik kırıkları: 77 hastanın değerlendirilmesi ve bir yaklaşım algoritması Yalçıner G, Kutluhan A, Bozdemir K, Çetin H, Tarlak B, Bilgen AS

Cilt - Vol. 18 Sayı - No. 5

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ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY C‹LT - VOL. 18

SAYI - NUMBER 5 EYLÜL - SEPTEMBER 2012

İçindekiler - Contents

429-435 The mid-term results of treatment for tibial pilon fractures Tibia pilon kırıklarında orta dönem cerrahi sonuçlarımız Gülabi D, Toprak Ö, Şen C, Avcı CC, Bilen E, Sağlam F 436-440 Early period psychiatric disorders following burn trauma and the importance of surgical factors in the etiology Yanık travması sonrası erken dönemde görülen psikolojik bozukluklar ve etyolojide cerrahi faktörlerin yeri Yabanoğlu H, Yağmurdur MC, Taşkıntuna N, Karakayalı H 441-445 Penetran kardiyak yaralanmalar: 21 olgunun değerlendirilmesi Penetrating cardiac injuries: assessment of 21 patients Dereli Y, Özdemir R, Ağruş M, Öncel M, Hoşgör K, Özdiş AS

Olgu Sunumu - Case Reports 446-448 A rare cause of small bowel obstruction in adults: persistent omphalomesenteric duct Erişkinlerde ince bağırsak tıkanıklığının nadir bir nedeni: Persistan omfalomezenterik kanal Güner A, Keçe C, Boz A, Kahraman İ, Reis E 449-452 Spontaneous migration of a retained bullet within the brain: a case report Beyin içinde kalan kurşunun kendiliğinden yer değiştirmesi: Olgu sunumu Arslan M, Eseoğlu M, Güdü BO, Demir İ, Kozan AB 453-454 The hidden devil: unexpected retained knife in the chest wall Gizli şeytan: göğüs duvarı içinde beklenmedik biçimde kalmış bıçak Chang CC, Lin HJ, Foo NP, Chen KT 455-457 Bilateral simultaneous anterior obturator dislocation of the hip by an unusual mechanism a case report Olağandışı bir mekanizmayla çift taraflı, eşzamanlı anterior obturator kalça çıkığı: Olgu sunumu Sultan A, Dar TA, Wani MI, Wani MM, Shafi S 458-460 Emergency surgery due to go-kart injuries: report of two consecutive cases Go-kart yaralanmalarına bağlı acil cerrahi: Ardışık iki olgunun sunumu Yılmaz KB, Akıncı M, Kaya O, Kulaçoğlu H 461-462 Isolated basal ganglia hemorrhage due to blast injury Blastik yaralanmaya bağlı izole bilateral bazal ganglion kanaması Aygün FM, Aygün MS, Önal MB, Demirci OL

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):367-375

Experimental Study

Deneysel Çalışma doi: 10.5505/tjtes.2012.59932

The effect of catheter use on vein grafting of a peripheral nerve defect: an experimental study Ven grefti ile periferik sinir defektlerinin onarımında kateter kullanımının sinir rejenerasyonuna etkisi: Deneysel çalışma Alper Mehmet BAYRAKTAR,1 Serhat ÖZBEK,2 Mesut ÖZCAN,2 Behzat NOYAN,3 İlkin ÇAVUŞOĞLU4 BACKGROUND

AMAÇ

Since vein grafts have been used in the repair of nerve defects, studies regarding this procedure have accumulated, and after coming into clinical use, it was noticed that there is a problem of collapse in the vein graft.

Sinir defektlerinin rekonstrüksiyonunda ven greftlerinin kullanılması ile ilgili çalışmaların artması ve bu uygulamanın klinikte kullanıma girmesiyle birlikte, ven greftinin kollabe olma sorununun ortaya çıktığı görülmüştür.

METHODS

GEREÇ VE YÖNTEM

Forty Sprague-Dawley rats were used, divided into five groups. No surgical intervention was performed in the first group. The defect was created in the sciatic nerve in Group 2 and left unrepaired. In Group 3, the defect was repaired with a nerve graft. In Group 4, the defect was repaired with a vein graft, while in Group 5, the repair was performed using a vein graft with an inserted catheter. In order to evaluate functional recovery and nerve regeneration, walking track analysis, electrophysiologic and histomorphometric analyses were done at the end of the 12th week.

Çalışmada 40 adet Spraque-Dawley sıçan kullanıldı. Beş gruptan, 1. gruba herhangi bir cerrahi girişim yapılmadı; 2. grubun siyatik sinirinde oluşturulan defekt onarılmadan bırakıldı, 3. grupta defekt sinir grefti ile onarıldı, 4. grupta defekt ven grefti ile 5. grupta ise ven grefti ve katater birlikte kullanılarak onarım yapıldı. Birinci ve ikinci grup kontrol grubu olarak kullanıldı. Fonksiyonel iyileşmeyi, sinir rejenerasyonunu değerlendirmek amacıyla, 12. haftanın sonunda, yürüme analizi, elektrofizyolojik ve histomorfometrik analizler yapıldı.

RESULTS

BULGULAR

Although there were no functional differences between Groups 5 and 4, comparisons regarding nerve conduction velocity demonstrated that the results obtained in Group 5 were better than those in Group 4. When the number of axons on the distal part of the sciatic nerve and mid-segment of the repaired area was taken into account, no significant difference was found between Groups 3 and 5, whereas there was a significant difference between Groups 4 and 5.

Defektin ven grefti ve katater ile onarıldığı grup (grup 5) ile grup 3 ve 4 arasında fonksiyonel açıdan fark bulunmazken, sinir iletim hızı açısından bakıldığında, 5. gruptaki sonuçlar, ven grefti ile onarım yapılan gruptan (grup 4) daha iyi bulundu. Onarım distalinden ve onarım alanının ortasından alınan siyatik sinir kesitlerindeki akson sayısına bakıldığında 3. ve 5. grup arasında fark bulunamazken; 4. ve 5. grup arasındaki fark anlamlıydı.

CONCLUSION

SONUÇ

In our study, it was experimentally shown that the problem of collapse of a vein graft occurring after its use in the reconstruction of a nerve defect can be overcome by placing a catheter into the vein graft. Consequently, this method may eliminate the need for the use of a nerve graft in selected cases. Key Words: Peripheral nerve injury; nerve defect; vein graft.

Department of Plastic and Reconstructive Surgery, Çekirge State Hospital, Bursa; Departments of 2Plastic and Reconstructive Surgery, 3Physiology, 4 Histology, Uludağ University Faculty of Medicine, Bursa, Turkey.

1

Bu çalışma sonucunda, ven grefti ile onarılan periferik sinir yaralanmalarında görülebilen ven grefti kollapsının ven grefti içine kateter yerleştirilmesi ile aşılabileceği ve bu sayede onarımda sinir grefti kullanma ihtiyacının ortadan kalkabileceği deneysel olarak gösterilmiştir. Anahtar Sözcükler: Periferik sinir yaralanması; sinir hasarı; ven grefti.

Çekirge Devlet Hastanesi, Plastik ve Rekonstrüktif Cerrahi Kliniği, Bursa; Uludağ Üniversitesi Tıp Fakültesi, 2Plastik ve Rekonstrüktif Cerrahi Anabilim Dalı, 3Fizyoloji Anabilim Dalı, 4Histoloji Anabilim Dalı, Bursa.

1

Correspondence (İletişim): Alper Mehmet Bayraktar, M.D. Çekirge Devlet Hastanesi, Osmangazi, Bursa, Turkey. Tel: +90 - 224 - 239 36 36 e-mail (e-posta): alperprc@yahoo.com

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The repair of a peripheral nerve injury is a challenging problem in reconstructive surgery. End-to-end repair is the first alternative, if the nerve ends can be approximated without undue tension. If there is a nerve defect, many technical procedures have been reported for the repair. Repair with autogenous nerve grafts, vascularized nerve grafts, autogenous vein grafts, use of synthetic tubes, and end-to-side nerve coaptations are the options.[1-3]

cal Committee of UludaÄ&#x; University. Forty female Sprague-Dawley rats weighing 225-300 g were used and maintained under standard laboratory conditions. The rats were randomly divided into five groups for different surgical treatments, except for the group consisting of animals with non-operated sciatic nerves. There were eight rats in each group. The animals were allowed free access to rat chow and water.

If end-to-end repair is not available, the use of a nerve graft is the gold standard in the repair of nerve defects.[4] Although nerve grafting has superior results, it also has some donor-site morbidities and usually necessitates preparation of a distant operation site and further dissection.[5-7]

Surgery was performed using a binocular operative microscope (MTX-1H1SVI; Olympus Optical Co., Ltd., Tokyo, Japan) and microsurgical techniques. After induction of sodium pentobarbital anesthesia (Nembutal, 30-50 mg/kg intraperitoneally; Abbott Laboratories, Quebec, Canada), temporary inhalational ether was provided during the electrophysiological studies. After the anesthesia, the left hind limbs of the rats were treated in a sterile manner.

If vein graft is not the choice, or in cases of absent proximal nerve stump, end-to-side nerve coaptation has been accepted as a reliable alternative method in nerve repair.[8,9] The main advantages of this method are to eliminate the need for a nerve graft and donor site morbidity and to locate the coaptation site and the target organ in close proximity. However, functional loss in the intact neighboring nerve that is used as a donor nerve remains controversial.[8,9] In the repair of nerve defects, the use of a vein graft is another alternative procedure.[10-12] In contrast to many resorbable nerve tube models, vein grafts have biologic permeability and are used as an alternative to nerve grafts in long segmental nerve defects.[13] Biologic permeability permits diffusion of the released neurotrophic factors and prevents fibrous tissue infiltration.[14] Since vein grafts have been used in the repair of nerve defects, studies regarding this procedure have been accumulated, and after coming into clinical use, it was found that there is a problem of collapse in the vein graft.[15-17] The best results are achieved after the repair of 3 cm or smaller defects due to the collapse of longer vein grafts.[17] Some researchers placed pieces of nerve [18-20] and muscle tissue[21,22] inside the vein graft to prevent the collapse of the graft, and they obtained good results in defects shorter than 3 cm with this combined technique.[18-20] The aim of this study was to place a catheter inside the vein graft to prevent the collapse of the graft occurring after its use in the reconstruction of a nerve defect. By using this technique, transition of proximal regeneration to the distal part is presumed to be complete and effective.

MATERIALS AND METHODS Animal Preparation This study was approved by the Animal Ethi368

Surgical Procedures

Skin and gluteal muscle were incised, and the sciatic nerve segment between the sciatic foramen and the bifurcation of tibial-peroneal branches was isolated from the neighboring tissues by separating membranous structures. The sciatic nerve was preserved at a level 7 mm distal to the sciatic foramen and at a level 7 mm proximal to its bifurcation (the common peroneal and tibial nerves). A 1.5 cm segment of sciatic nerve located in the middle was excised to create a nerve defect. This procedure was applied to all experimental groups except Group 1. Additionally, in Groups 4 and 5, after reaching the external jugular vein by a 3 cm vertical skin incision, a segment of vein 20 mm in length was obtained. In Group 1, the sciatic nerves of the animals were not operated and were used to obtain normative data (Fig. 1). In Group 2, the sciatic nerve defect was not repaired and both ends of the defect were buried into nearby muscles using nylon stitches (Fig. 1). In Group 3, the excised nerve segment was rotated 180° and sutured to its own place as a nerve graft (Fig. 1). In Group 4, the nerve defect was repaired using a vein graft (Fig. 1). In Group 5, the repair was performed by placing a catheter inside the vein graft (Fig. 1). After the catheter was placed into the vein graft in Group 5, the distal part of the catheter was taken out distal to the graft-nerve anastomosis line. In order to be able to remove the catheter in the postoperative period, a second catheter was placed into a point close to the m. gluteus superficialis insertion. The proximal part of each catheter was removed out of the neck by passing it through subcutaneous tissue (Fig. 2). Eylßl - September 2012


The effect of catheter use on vein grafting of a peripheral nerve defect

D

P

D

(a)

P

(b) D

D

P

(c)

D

P

(e)

P

(d)

Fig. 1. Experimental Groups: (a) Group 1, non-operated sciatic nerve group, normative data was obtained, (b) Group 2, defect group that was not repaired, (c) Group 3, the excised nerve segment was rotated 180簞 and sutured to its own place to be used as a nerve graft, (d) Group 4, nerve defect was repaired by using a vein graft, and (e) Group 5, the repair was performed placing a catheter inside the vein graft. D: Distal; P: Proximal.

After the first postoperative week, catheter no. 1 was pulled out through catheter no. 2 stepwise every second day according to the mean rate of neural regeneration in rats, which was considered to be 2.5-3 mm/day.[23] Ether anesthesia was used during this manipulation. Total removal of the catheters necessitated three steps by pulling 5 mm at each step, and in the third step, both catheters were removed. All coaptations were performed using 10-0 nylon sutures. Muscle incisions were sutured with 4-0 absorbable materials, and the skin was closed with 4-0 nylon sutures. (a)

Gait Analysis Twelve weeks after the surgical procedures, a gait analysis was performed for all of the rats. The hind paws of each rat were soaked in methylene blue solution, and the rat was allowed to walk on a paper that had been placed on the bottom of a walking track to provide a paw print record. The procedure was repeated when the results were unsatisfactory. A sciatic functional index (SFI) was calculated for each rat using the following formula (reported by Brown et al.):[24,25] Sciatic Functional Index = -38.3 ([EPL-NPL]/

(b)

Catheter 1 Catheter 2

Sciatic nerve Vien graft

(c)

(d)

Fig. 2. The catheter used in Group 5 was placed into the vein graft, and the distal part of the catheter was taken out distal to the graft-nerve anastomosis line (a). In order to be able to remove the catheter in the postoperative period, a second catheter was placed into a point close to the m. gluteus superficialis insertion (b). The first catheter was placed into the second catheter in order to obtain controlled removal. The proximal portion of each catheter was removed from the neck by inserting it through the subcutaneous dissection plane of rats (c). (d) A schematic drawing of this method. Cilt - Vol. 18 Say覺 - No. 5

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NPL) + 109.5 ([ETS-NTS]/NTS) + 13.3 ([EIT-NIT]/ NIT)-8.8, Where EPL=Experimental print length, NPL=Normal print length, ETS=Experimental toe spread (first–fifth toe), NTS=Normal toe spread, and EIT=the indices. SFIs were calculated by an investigator blinded to the experimental conditions. An index of 0 reflects normal function and an index of -100 represents complete loss of function.[24-26] Electrophysiological Tests After the walking track procedure, the rats were anesthetized with temporary inhalation of ether, reincision was made on the left hind limb, and the nerves were exposed and dissected carefully. Following exposure of the nerves, nerve conduction velocity (NCV) for the sciatic nerve in each animal was measured in all groups using MP 100 data acquisition and analysis system (Biopac Systems Inc., CA, USA). During these measurements, stimulating electrodes were placed under the sciatic nerve proximal to the suture line (7 mm away), and recorder electrodes were placed under the distal part of the sciatic nerve, at the division of tibial and peroneal nerve branches (7 mm away). Supramaximal stimulus (7 V, 0.5-msec duration) generated by an MP 100 stimulator was used to stimulate the nerve, and the distance between the electrodes was measured. NCV was calculated by quotient of distance with time recorded as m/sec. Histomorphometric Assessment Following the electrophysiological measurements, the animals were sacrificed by high dosage of anesthetic agent and sciatic nerves were removed, 5 mm proximal to the proximal anastomosis line and 5 mm distal to the distal anastomosis line. A single nerve tissue sample was taken from Group 1; nerve tissue samples from the medial part of grafted sites as well as from proximal and distal parts were taken from all groups except for those in Group 2 (Fig. 3).

D

P

Group 1

D

P

Group 2

D

P

Group 3

D

P

Group 4

D

P

Group 5

Shows the level of histologic section taken from each group

Fig. 3. Schematic drawing of experimental groups and histological sections. D: Distal; P: Proximal.

software (Scion Corp., Frederick, MD) were used to capture images, and the image analysis system was calibrated using a hemocytometer before measurements were obtained. Ten microscopic fields, selected randomly, were then captured for each nerve sample through an objective (magnification X40; Nikon, Tokyo, Japan) for accurate recognition and counting of the myelinated nerve fibers. Accounting frame of the known area was created using Scion-Image software and superimposed on the digital image to be counted. Myelinated axons were then quantified according to the unbiased counting rule[27] and results expressed as area densities of myelinated axons (axons per square millimeter). Statistical Analysis

Harvested tissue samples were fixed in 4% glutaraldehyde in 0.1 M phosphate buffer at pH 7.4. Each sample was then postfixed with 1% OsO4 in 0.1 M phosphate buffer for 2 hours, dehydrated through a graded series of ethanol, and embedded in Spurr resin (Agar Scientific, Stansted, UK). Semi-thin (0.5 µm) sections of the entire nerve perpendicular to the long axis of the nerve fibers were then obtained and stained with a mixture of 1% toluidine blue and 1% borax in distilled water.

Concurrency of the variable values to normal distribution was initially tested by a one-sample Kolmogorov-Smirnov test to decide whether to use parametric or nonparametric tests. Functional and electrophysiologic evaluation results and axon numbers were evaluated by Mann-Whitney U and Kruskal-Wallis tests using the Statistical Package for the Social Sciences (SPSS) 13.0 program. Pearson correlation test was used for correlation of intergroup variables with one another.

A digital camera (Cybershot DSC-F717; Sony, Tokyo, Japan) attached to a light microscope (4S-2 Alphaphot; Nikon, Tokyo, Japan) and Scion Image

All of the quantitative results were expressed as ± standard error and the result of p<0.05 was considered significant in the statistical analysis.

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0

Group 1

Group 2

Group 3

Group 4

Group 5

-20 -40 -60

60

45 30

15

-80 0 -100

Fig. 4. Comparison with respect to Sciatic Functional Index.

RESULTS Twelve weeks after the surgery, all of the rats in Groups A, B, C, D, and E were subjected to walking track analysis. -100 showed whole function loss and 0 showed normal function. The SFI was found as 0 in the control group (Group 1), -83.038±6.93 in Group 2, -52.8±14.10 in Group 3, -63.33±13.26 in Group 4, and -53.78±20.70 in Group 5, respectively (Fig. 4). When groups were compared with Kruskal-Wallis test, it was found as p<0.01, that is, at least one group was different from the others. The groups were then evaluated among themselves using Mann-Whitney U test. There were statistically significant differences between Groups 2 and 3 (p<0.01), Groups 2 and 4 (p<0.05) and Groups 2 and 5 (p<0.01). Conversely, no statistically significant differences were found between Groups 3 and 4, Groups 3 and 5 and Groups 4 and 5. Although the difference between Groups 4 and 5 was not found statistically important (p>0.05), there was a considerable difference in parameters (p=0.08) (Fig. 4). Average NCV was found as 51.08±1.85 in Group 1, 43.2±1.87 in Group 3, 42.54±2.22 in Group 4 and 50.7±3.24 in Group 5, respectively. No NCV could be measured in Group 2 (Fig. 5). While there was a statistically significant difference between Groups 1 and 3 and Groups 1 and 4 (p<0.01), no significant difference was found between Groups 1 and 5 (p>0.05). Similarly, the difference between Groups 3 and 4 and between Groups 3 and 5 was not significant. However, the difference between Groups 4 and 5 (p<0.01) was of value (Fig. 5). During histomorphometric evaluation, as shown in Fig. 3, different nerve tissue samples were taken from different levels in different groups. When examined in terms of proximal sections, no statistically significant difference was determined between Groups 1 and 2 with regard to mean values of myelinated axon number. At the same time, no statistically significant difference was determined between Groups 3-4 and Cilt - Vol. 18 Sayı - No. 5

Group 1

Group 2

Group 3

Group 4

Group 5

Fig. 5. Comparison with respect to nerve conduction velocities in all groups. 15000

Axon/mm2

Axon/nerve

12000 9000 6000 3000 0

Group 1

Group 2

Group 3

Group 4

Group 5

Fig. 6. Comparison of histomorphometry of sciatic nerve proximal sections. 15000

12000

9000

6000

3000 0

Group 1

Group 2

Axon’mm2 (Mid section) Axon/Nerve (Mid section)

Group 3

Group 4

Group 5

Axon/mm2 (Distal section) Axon/Nerve (Distal section)

Fig. 7. Comparison with respect to histomorphometric analysis. Bar graph showing the number of myelinated axons per square millimeter and nerve unit area observed in medial and distal sections from rats in Groups 1, 3, 4, and 5 12 weeks after surgical procedures. (Histomorphometric analysis was not performed in Group 2 due to the lack of myelinated fibers in tissue samples from this group.)

5 (p>0.05). On the contrary, the difference between Groups 1-2 and 3-4-5 was significant (p<0.05) (Fig. 6). 371


Ulus Travma Acil Cerrahi Derg

(a)

(b) Fig. 8. Photographs of (a) medial, and (b) distal sections of Groups 3-4 and 5.

For the histomorphometry of medial and distal nerve sections, the number of myelinated axons in the sciatic nerve in Groups 3 and 5 was comparatively higher compared to the positive control group (Group 1) (p<0.001), but there was no significant difference between Groups 3 and 5. In Group 5, the number of myelinated axons in the distal sciatic nerve section was comparatively higher compared to Group 4, and the difference was statistically significant (p<0.05) (Fig. 7, 8). Similarly, the difference between Groups 3 and 4 was significant (p<0.05) (Fig.7, 8). For Group 2, myelinated axons were not found in distal sciatic nerve sections, and histomorphometric analysis was not performed in this group. In Groups 3 and 5, in spite of the high number of myelinated axons in distal nerve sections, axon diameters were smaller than normal. Similarly, when the number of axons was examined in medial and distal sections for each mm2, Groups 3 and 5 had higher axon numbers compared to Group 4, which was statistically significant (p<0.05) (Fig. 7, 8).

DISCUSSION The repair of a nerve defect is one of the important problems of reconstructive surgery. Although the use of a nerve graft in the repair of a nerve defect is the main choice,[1-4] some problems faced during acquisition of an available nerve, and resulting donor site morbidity, limit its use.[5-7] The use of a vein graft in 372

such defects is another preferred surgical method.[10] As the use of vein grafts in reconstruction of a nerve defect became popular and gained a place in clinical practice,[10-12] it was observed that vein grafts used in this procedure have a problem of collapse.[17] Autogenic vein grafts are supportive tunnels for regeneration and maturation of nerve fibers that are experimentally and clinically proven.[10] Developing the skeleton structure of nerve buds emerging from regenerated nerve ends, providing axonal migration, possessing extracellular matrix contents, and utilizing them with the help of growth factors, vein grafts are shown to have all conditions for nerve conduit models. [2] Chiu[10] and Walton[11] reported successful results on this subject. Contrary to many resorbable nerve conduit models that are used for nerve defect repairs, vein grafts are alternatives for nerve grafts in long defects because of their biological permeability. This current biological permeability has an advantage of allowing the diffusion of neurotrophic factors and preventing fibrous tissue infiltration. Nowadays, the most important problem of synthetic and resorbable nerve conduit models and tissue engineers is providing biological permeability.[14] The elastic structure of the vein prevents formation of adhesion and scar tissue and also formation of compression. Eyl端l - September 2012


The effect of catheter use on vein grafting of a peripheral nerve defect

Because vein grafts are non-immunogenic, they form less inflammatory reaction. Obtaining vein grafts is easier, they last longer than bioabsorbable nerve conduits, and they have many alternatives for diameter tunes.[15] After nerve regeneration, because the vein is an autogenous tissue, there is no need for taking the vein out of the surgical area.[10] The three layers of veins are rich in laminin, and this shows similarity with basal lamina that surrounds normal or traumatized nerve fibers. Laminin takes a part in adhesion, multiplication and differentiation of nerve cells. [16] Despite all the advantages of vein grafts, the serious problem repairing nerve defects with vein grafts is collapse, especially in long defects.[17] Some researchers used vein grafts filled with muscle tissue[21,22] or divided nerve tissue[18-20] to prevent collapse, but best results with this combined technique were obtained in defects that were shorter than 3 cm. In this experimental study, a catheter was placed into a vein graft in order to overcome the collapse problem. The rate of drawback of the catheter from the distal coaptation point was arranged due to “delaying time in scar”[23,28,29] and nerve regeneration rate [23,28,29] in rats and vein graft length. Therefore, we not only prevented collapse but also obtained necessary, adequate nerve tube length for the regeneration. Furthermore, by drawing the catheter back, the rate of the regeneration was not delayed and the foreign body reaction was probably reduced. In experimental nerve repair models, histology, morphometry, electron microscopy, NCV measurement, muscle mass index, and electromyelography have been used to determine the quantity and quality of nerve regeneration.[24,30,31] In order to determine the regeneration functionally, SFI obtained by walking analysis and peroneal functional index have been used.[24,30,31] When our study is evaluated in terms of nerve functional index, especially the relationship between Groups 3, 4 and 5 was investigated, and groups were compared both among themselves and to control groups. Even though there was a statistically significant difference between Group 2 and Groups 3-4-5, respectively, it was accepted as an estimated result. Despite the fact that no statistically significant difference was determined among groups when comparing Groups 3-4-5, the considerable difference in parameters between Group 4 and Groups 3-5 suggests that if the study is conducted in larger series, it may change in favor of Group 3 and Group 5. Compared with other evaluation tests, SFI is the best method in the evaluation of function and clinical period since it depends on sensory and muscle function.[24,32] Nerve conduction velocity (NCV) and morphometCilt - Vol. 18 Sayı - No. 5

ric analysis cannot reflect functional healing, which is the main aim of peripheral nerve surgery. When epineural suture technique is performed during the repair, axons in the proximal stump sprout through the distal endoneural tube, and therefore, NCV measurement done with electrical stimulation gives a positive result. However, if the regenerated axons reaching the distal stump cannot reach the target organ, a suitable functional result will not appear, although there is an electrical flow throughout the nerve.[33,34] When this condition is taken into account, the fact that the parameters in Group 3 and Group 5 demonstrated noticeable differences compared with Group 4 shows good promise for our study. When the results of NCV were examined, a statistically significant difference was found between Group 1 and Groups 3 and 4. The fact that the nerve graft of the control group was significantly good compared to that of the vein graft was not surprising. Whereas the superiority of Group 5 to the nerve graft group (Group 3) could not be shown, the statistically significant difference that could be obtained between Group 5 (catheterized vein graft group) and Group 4 (vein graft group) was of importance. The reason for this result was that the number of axons reaching the repair site and distal region in the vein graft group with catheter was more than in the vein graft group. In histomorphometric measurements, proximal sections were examined first. No significant difference was present between Groups 1 and 2, whereas a statistically significant difference was present compared to Groups 3, 4 and 5. No statistically significant difference could be determined between Groups 3, 4 and 5. These findings were normal as they should regenerate after nerve damage. The number of axons in the nerve in Groups 3, 4 and 5 was consistent with regeneration findings, which takes place in a damaged nerve. There were a number of myelinated axons and nerve clumps that were in smaller dimensions; axons without myelin were also present and numbered more than in the control group. The distal and medial sections, which are of importance in terms of the result of our study, were examined with regard to the number of the axons in the nerve. Whereas no significant difference could be found between the nerve graft group (Group 3) and Group 5 in which a catheter was placed into the vein graft, it was observed that the differences between Groups 3 and 4 (vein graft group) and between Groups 5 and 4 were statistically significant. The fact that the difference occurring in favor of Group 3 between the nerve graft group (Group 3) and vein graft group (Group 4) was not present between Group 3 and Group 5 (vein graft group with catheters) is due to the positive effects of the catheter placement. 373


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The results in all tests, except in SFI, were in favor of nerve graft and catheterized vein graft. In this experimental study, we aimed to overcome the collapse problem of the vein graft by using an enclosed catheter. When it is considered that the problem of vein collapse usually occurs when the gap is longer than 3 cm (as mostly seen in clinical procedures),[17] this study cannot contribute to the literature because the maximum length of a sciatic nerve defect cannot exceed 3 cm in a rat model. Unfortunately, standard scientific tests that can be used to evaluate nerve regeneration in bigger animal models, such as in dogs or monkeys, are not available. The model used in this study, in which nerve defects were repaired by placing a catheter into a vein graft, has the following advantages: 1) In cases where obtaining an ideal and extremely acceptable nerve graft is difficult, vein grafting is a procedure in which a vein graft can be obtained easily, and the technical application is easy. Diameter adaptation is not necessary, and the graft is non–immunogenic. As the vein is an autogenic tissue, it is not necessary to remove the vein from the surgical site after the completion of nerve regeneration. 2) Donor site morbidity is minimal compared to nerve grafting. 3) The collapse problem of the vein graft can be overcome by catheter placement into the vein, and it seems possible to use this technique in 3 cm and longer nerve defects. 4) Micro biological media occurring in the vein graft and axoplasmic fluid accumulation at the graft site are useful and valuable for nerve regeneration. 5) Compared to synthetic nerve tube models, biologic permeability of the vein graft is one of its advantages. With this experimental study, sciatic nerve defect repair done by a vein graft with an enclosed catheter demonstrated better results compared to single vein graft application. This procedure may eliminate the need for a nerve graft to repair a peripheral nerve defect and the risk of a functional loss in the donor nerve. In cases where nerve defect repair is planned to be performed using a vein graft, the collapse problem of the vein graft, which constitutes a serious problem, may be overcome with this method. However, to date, no adequate data are present for its clinical use.

REFERENCES 1. Payne SH Jr. Nerve repair and grafting in the upper extremity. J South Orthop Assoc 2001;10:173-89. 2. Thomas MB. Nerve repair and grafting, In Green DP, Hotchkiss RN, Pederson WC, editors. Green’s operative hand sur374

gery. Vol 2., Philadelphia: Churchill Livingstone; 1999. p. 1381-404. 3. Sunderland S. The anatomy and physiology of nerve injury. Muscle Nerve 1990;13:771-84. 4. IJkema-Paassen J, Jansen K, Gramsbergen A, Meek MF. Transection of peripheral nerves, bridging strategies and effect evaluation. Biomaterials 2004;25:1583-92. 5. Lundborg G, Dahlin JB. Structure and function of peripheral nerve. In: Gelberman RH, editor. Operative nerve repair and reconstruction. Philadelphia: JB Lippincott; 1991. p. 3-18. 6. Lundborg G. Nerve regeneration and repair. A review. Acta Orthop Scand 1987;58:145-69. 7. Brandt KE, Mackinnon SE. Microsurgical repair of peripheral nerves and nerve grafts. In: Aston SJ, Beasley RW, Tho CHM, editors. Grabb and Smith’s plastic surgery. Philadelphia: Lippincott-Raven; 1997. p. 79-90. 8. Liu K, Chen LE, Seaber AV, Goldner RV, Urbaniak JR. Motor functional and morphological findings following end-to-side neurorrhaphy in the rat model. J Orthop Res 1999;17:293300. 9. Ozbek S, Ozcan M, Noyan B, Kurt MA, Tirelioğlu S, Bozkurt C, et al. End-to-side nerve coaptation: is an additional proximal coaptation useful when available? Ann Plast Surg 2005;55:281-8. 10. Chiu DT, Janecka I, Krizek TJ, Wolff M, Lovelace RE. Autogenous vein graft as a conduit for nerve regeneration. Surgery 1982;91:226-33. 11. Walton RL, Brown RE, Matory WE Jr, Borah GL, Dolph JL. Autogenous vein graft repair of digital nerve defects in the finger: a retrospective clinical study. Plast Reconstr Surg 1989;84:944-9; discussion 950-2. 12. Chiu DT, Strauch B. A prospective clinical evaluation of autogenous vein grafts used as a nerve conduit for distal sensory nerve defects of 3 cm or less. Plast Reconstr Surg 1990;86:928-34. 13. Mackinnon SE, Dellon AL. Clinical nerve reconstruction with a bioabsorbable polyglycolic acid tube. Plast Reconstr Surg 1990;85:419-24. 14. Hudson TW, Evans GR, Schmidt CE. Engineering strategies for peripheral nerve repair. Clin Plast Surg 1999;26:617-28. 15. Foidart-Dessalle M, Dubuisson A, Lejeune A, Severyns A, Manassis Y, Delree P, et al. Sciatic nerve regeneration through venous or nervous grafts in the rat. Exp Neurol 1997;148:236-46. 16. Thanos PK, Okajima S, Terzis JK. Ultrastructure and cellular biology of nerve regeneration. J Reconstr Microsurg 1998;14:423-36. 17. Chiu DT. Autogenous venous nerve conduits. A review. Hand Clin 1999;15:667-71. 18. Tang JB. Group fascicular vein grafts with interposition of nerve slices for long ulnar nerve defects: report of three cases. Microsurgery 1993;14:404-8. 19. Tang JB. Vein conduits with interposition of nerve tissue for peripheral nerve defects. J Reconstr Microsurg 1995;11:216. 20. Keskin M, Akbaş H, Uysal OA, Canan S, Ayyldz M, Ağar E, et al. Enhancement of nerve regeneration and orientation across a gap with a nerve graft within a vein conduit graft: a functional, stereological, and electrophysiological study. Plast Reconstr Surg 2004;113:1372-9. 21. Battiston B, Tos P, Cushway TR, Geuna S. Nerve repair by means of vein filled with muscle grafts I. Clinical results. Microsurgery 2000;20:32-6. Eylül - September 2012


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22. Battiston B, Tos P, Geuna S, Giacobini- Robechi MG, Guglielmone R. Nerve repair by means of vein filled with muscle grafts. II. Morphological analysis of regeneration. Microsurgery 20: 37–41, 2000. 23. Danielsen N, Lundborg G, Frizell M. Nerve repair and axonal transport: outgrowth delay and regeneration rate after transection and repair of rabbit hypoglossal nerve. Brain Res 1986;376:125-32. 24. Varejão AS, Meek MF, Ferreira AJ, Patrício JA, Cabrita AM. Functional evaluation of peripheral nerve regeneration in the rat: walking track analysis. J Neurosci Methods 2001;108:1-9. 25. Brown CJ, Mackinnon SE, Evans PJ, Bain JR, Makino AP, Hunter DA, et al. Self-evaluation of walking-track measurement using a Sciatic Function Index. Microsurgery 1989;10:226-35. 26. Hare GM, Evans PJ, Mackinnon SE, Best TJ, Bain JR, Szalai JP, et al. Walking track analysis: a long-term assessment of peripheral nerve recovery. Plast Reconstr Surg 1992;89:2518. 27. Mayhew TM. A review of recent advances in stereology for quantifying neural structure. J Neurocytol 1992;21:313-28.

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28. Lundborg G. A 25-year perspective of peripheral nerve surgery: evolving neuroscientific concepts and clinical significance. J Hand Surg Am 2000;25:391-414. 29. Amara B, de Medinaceli L, Lane GB, Merle M. Functional assessment of misdirected axon growth after nerve repair in the rat. J Reconstr Microsurg 2000;16:563-7. 30. Al-Qattan MM. Terminolateral neurorrhaphy: review of experimental and clinical studies. J Reconstr Microsurg 2001;17:99-108. 31. Bain JR, Mackinnon SE, Hunter DA. Functional evaluation of complete sciatic, peroneal, and posterior tibial nerve lesions in the rat. Plast Reconstr Surg 1989;83:129-38. 32. Weber RA, Warner MR, Verheyden CN, Proctor WH. Functional evaluation of gap vs. abutment repair of peripheral nerves in the rat. J Reconstr Microsurg 1996;12:159-63. 33. Giovanoli P, Koller R, Meuli-Simmen C, Rab M, Haslik W, Mittlböck M, et al. Functional and morphometric evaluation of end-to-side neurorrhaphy for muscle reinnervation. Plast Reconstr Surg 2000;106:383-92. 34. Kanaya F, Firrell JC, Breidenbach WC. Sciatic function index, nerve conduction tests, muscle contraction, and axon morphometry as indicators of regeneration. Plast Reconstr Surg 1996;98:1264-74.

375


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):376-383

Experimental Study

Deneysel Çalışma doi: 10.5505/tjtes.2012.45381

Comparison of topical zinc oxide and silver sulfadiazine in burn wounds: an experimental study Yanık yarası tedavisinde topikal çinko oksit ile gümüş sülfadiazinin karşılaştırılması: Deneysel çalışma Kemal ARSLAN,1 Ömer KARAHAN,1 Ahmet OKUŞ,1 Yaşar ÜNLÜ,2 Mehmet Ali ERYILMAZ,1 Serden AY,1 Barış SEVİNÇ1

BACKGROUND

AMAÇ

We aimed to compare the effects of topical zinc oxide and topical silver sulfadiazine in the treatment of partial-thickness burn wounds.

Bu çalışmada, yanık yaralarında yaygın olarak kullanılan çinko oksit ve gümüş sülfadiazinin tedavi etkileri karşılaştırıldı.

METHODS

GEREÇ VE YÖNTEM

The study was conducted with 20 New Zealand rabbits, and burn wounds were created by a brass probe. The animals were randomly divided into two groups. The burns were treated with zinc oxide (Group O) or silver sulfadiazine (Group S) with daily application. The wound healing process was followed both clinically and histopathologically. We determined the days at which 50% and 80% re-epithelization was observed.

Yeni Zelanda cinsi 20 tavşanda pirinç propla yanık yarası oluşturuldu. Tavşanlar rastgele iki gruba ayrıldı. Yanıklar günlük uygulamayla birinci grupta çinko oksitle (Grup O), ikinci grupta (Grup S) gümüş sülfadiazinle tedavi edildi. Yara iyileşmesi klinik ve histopatolojik olarak takip edildi. Yara ölçümleri yapıldı ve %50 ve %80 reepitelizasyona ulaştığı günler belirlendi.

RESULTS

Ortalama %50 ve %80 reepitelizasyona ulaşma süreleri Grup O’da sırasıyla 21,4 ve 25,4 gün, Grup S’de 25,8 ve 30,2 gündü (p<0,001). Yara kolonizasyonu ise 1, 2, 3, 4, 5 ve 6. haftalarda ortalama olarak Grup O’da daha düşüktü. Fark 2, 3, 4 ve 6. haftalarda anlamlı idi (p<0,001). Histopatolojik değerlendirme sonucunda Grup O’da epidermis, dermis ve skar dokusunun kalınlıkları sırasıyla 0,12, 3,80 ve 2,44 mm idi. Grup S’de ise 0,16, 4,76 ve 3,16 mm olarak bulundu (p<0,001).

The mean time for 50% and 80% re-epithelization was 21.4 and 25.4 days in Group O and 25.8 and 30.2 days in Group S, respectively (p<0.001). The mean score for wound colonization was lower in Group O. The difference was statistically significant at weeks 2, 3, 4, and 6 (p<0.001). In the histopathological examination, the thicknesses of the epidermis, dermis and scar tissue were 0.12 mm, 3.80 mm and 244 mm in Group O, and 0.16 mm, 4.76 mm and 3.16 mm in Group S, respectively (p<0.001). CONCLUSION

In this experimental burn study, zinc oxide was more effective than silver sulfadiazine in terms of epithelization, dermis maturation and scar formation.

BULGULAR

SONUÇ

Bu deneysel çalışmada, çinko oksit yanık tedavisinde epitelizasyon, epidermis maturasyonu ve skar oluşumunda gümüş sülfadiazinden daha etkili bulunmuştur.

Key Words: Zinc oxide; silver sulfadiazine; partial-thickness burn.

Anahtar Sözcükler: Çinko oksit; gümüş sülfadiazin; parsiyel kalınlıktaki yanık.

Presented at the 8th Turkish Congress of Trauma and Emergency Surgery (September 14-18, 2011, Antalya, Turkey).

8. Ulusal Travma ve Acil Cerrahi Kongresi’nde sunulmuştur (14-18 Eylül 2011, Antalya).

Departments of 1General Surgery, 2Pathology, Konya Training and Research Hospital, Konya, Turkey.

Konya Eğitim ve Araştırma Hastanesi, 1Genel Cerrahi Kliniği, 2 Patoloji Bölümü, Konya.

Correspondence (İletişim): Kemal Arslan, M.D. Necip Fazıl Mah., Ateşbazı Sok., Meram Yeniyol, 42040 Meram, Konya, Turkey. Tel: +90 - 332 - 323 67 09 e-mail (e-posta): arslanka74@hotmail.com

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Comparison of topical zinc oxide and silver sulfadiazine in burn wounds

In the treatment of burns, the aim is to treat burns, prevent infections and achieve the best functional and aesthetic results in a shorter time with lower costs. While healing burn wounds, a topical agent should decrease the rates of mortality and morbidity by preventing bacterial contamination and sepsis. The agent should also be easily accessible. An ideal agent with those properties has yet to be marketed. In the topical treatment of burn wounds, 1% silver sulfadiazine (SSD) pomade is the most commonly used agent worldwide.[1] SSD has been shown to decrease bacterial contamination, to hasten epithelization and to delay wound contraction.[2-8] However, SSD is also known to delay wound healing and separation of scar tissue, to cause atrophic and hypertrophic scars, especially more than three weeks after the applications, to have renal toxicity, to cause leukopenia, and to carry a risk for resistance.[9-19] Zinc is an essential element for the human body, and at the meeting of the World Union of Wound Healing Societies in Paris in 2004, it was accepted as having potential benefits in wound healing.[20] There are studies showing the benefits of systemic and topical use of zinc in wound healing. It is also reported that zinc accelerates the wound healing process when applied on open wounds.[21] To our knowledge, no study exists in the literature comparing the effects of local application of SSD and oxide zinc ointment (OZO) in burn wounds. Therefore, the present study was designed to compare the effects of topical SSD and OZO in experimental partial-thickness burns in rabbits.

MATERIALS AND METHODS Study design Permission was obtained from the ethical board of Meram Medical School of Selçuk University. The study was designed under the criteria of the Health Guide for the Care and Use of Laboratory Animals by the National Institutes of Health (NIH Publication No: 86-23, Revised 1985 Bethesda). The research was conducted at the Experimental Research Center of Selçuk University. The weight of rabbits ranged from 3200-3600 g. The rabbits were accommodated in a 12/12 hour light and dark cycle at 22-26°C and fed with a standard rabbit diet. As an analgesic, 100 mg/5 ml of ibuprofen was administered via drinking water after the formation of burns. The rabbits were accommodated individually and approached with appropriate equipment to prevent contamination. Before the study, punch biopsies as samples were obtained from eight rabbits to determine the thicknesses of normal epidermis and dermis. Mean values obtained from these samples were accepted as normal Cilt - Vol. 18 Sayı - No. 5

values. Partial-thickness burns were formed in 20 adult New Zealand rabbits. The rabbits were divided into two groups. OZO 20% was used in Group 1 (Group OZO), and SSD 1% was used in Group 2 (Group SSD). The healing period was followed up clinically and histopathologically. Five parameters were used in the determination of wound healing: 1. Days when 50% and 80% of re-epithelization was observed. 2. The score for wound colonization. 3. The histopathologic thickness of the epidermis. 4. The histopathologic thickness of the dermis. 5. The histopathologic thickness of the scar issue. Burn formation Anesthesia was achieved by a single dose of intramuscular 6 mg/kg of xylazine hydrochloride (Rompun, Bayer, 23.32 mg/ml) and 50 mg/kg of ketamine hydrochloride (Ketalar, Parke-Davis, 50 mg/ml). The back region of the rabbits was shaved and cleaned with 10% of povidone-iodine solution (Kim-Pa, Poviiodeks, 10% povidone-iodine). A specially designed brass probe with 10 cm² of surface area (2.5x4 cm diameter) was used for the formation of burns (Fig. 1a). Having been sterilized in boiling water for 5 minutes, the probe was applied to the skin of anesthetized rabbits for 15 seconds with no pressure. Using this procedure, second-degree partial-thickness burns were formed (Figs. 1b, c). After the formation of burns, all the rabbits were placed and kept in individual cages. Local treatment Group O was treated with OZO and Group S with SSD. OZO was formed with 20% zinc oxide and 80% Vaseline. OZO can be found commercially as 20% of Oxide de Zinc (ORO zinc cream, ORO drugs). SSD was formed from 1% SSD and 99% paraben, and can commercially be found as 1% Silvadiazin cream (Toprak Drug Co.). According to our treatment protocol, the drugs were administered as a thin layer on the wounds once per day. Then, all wounds were protected with non-stick cotton and sterile gauze with adhesive elastic bandage (Setanet® No: 3) and changed on a daily basis (Fig. 1d). Assessment of wound healing This study was continued for six weeks after the formation of burns. Each wound was clinically observed meticulously, and digital photos were taken with a camera (Sony® CyberShot DSC-W120) every three days during the following six weeks. At week 6, skin samples were collected, and wounds were as377


Ulus Travma Acil Cerrahi Derg

(a)

(c)

(b)

(d)

Fig. 1. The application of brass and burn formation.

sessed histologically. All the clinical and histological assessments of wounds were performed in a blinded fashion. At every change of dressings, wound healing was examined by an experienced clinician (a surgeon in the burn unit), and general comments were recorded (Fig. 2).

1. Assessment of re-epithelization During the study, the photos of wounds were taken once every three days after cleaning with serum physiologic. The photos were taken from a distance of 20 cm, in the same room under the same lighting conditions by the same researcher. The photos were

Fig. 2. Burn wounds on days 3, 14, 28, and 42.

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Reepithelization 50%

40

30

15 10 5

25 (mm)

20

20 15

Silver sulfadiazine

1.5

10 0.5

0

Zinc oxide

0

Silver sulfadiazine

Fig. 3. Times to 50% and 80% re-epithelization.

evaluated under the criteria of NIH Image J program (Image J ver: 1.44p, Wayne Rasband, NIH, USA). The margins of burn areas were marked and measured, and the measurements were recorded. The rate of reepithelization areas was calculated with the following formula: Percentage of re-epithelization = first burn area – current burn area ∕first burn area. The days on which 50% and 80% of re-epithelization was observed were detected for each rabbit. 2. Assessment of wound colonization Wound colonization was assessed according to exudation, purulent efflux, efflux odor, erythema, and edema. A score between 0 and 3 was given to each assessment as follows: 0: No finding of colonization, 1: Mild exudation and odor, 2: Erythema, moderate purulent efflux, exudation, and odor, and 3: Severe exudation, purulent efflux, odor, edema, and erythema. Each assessment was performed by the same blinded researcher, who was unaware of the scores of rabbits determined before and during the treatment. 3. Histopathological assessment The study was continued for six weeks and discontinued at the end of week 6. At the end of the study, all the rabbits were sacrificed after their photos were taken. Full-thickness skin samples at burn areas were resected. Skin samples were preserved in formaldehyde solution and stained with hematoxylin-eosin (HE) and Masson trichrome dyes. The thicknesses of the epidermis, dermis and scar tissues were blindly evaluated through the NIH Image J program. In the assessment, the biopsy results of healthy rabbits prior to the study were accepted as normal values. Statistical analysis Collected data were analyzed using the Statistical Package for the Social Sciences (SPSS) 13.0 for Windows program. The values were evaluated as Cilt - Vol. 18 Sayı - No. 5

Silver sulfadiazine

1

5 Zinc oxide

Zinc oxide

2

30

1. week

2. week

3. week

4. week

5. week

6. week

Fig. 4. Wound colonization in the OZO and SSD groups. Epidermis 0.18 0.16 0.14 (mm)

Days postburn injury

Days postburn injury

2.5

30

25

0

Reepithelization 80%

0.12 1 0.08 0.06 0.04 0.02 0

Zinc oxide

Silver sulfadiazine

Fig. 5. Mean epidermis thickness in both groups (mm).

mean±SD. Student’s t test was used for comparison of the groups. A p value lower than 0.05 was accepted to be significant.

RESULTS At the beginning of the study, all the burn wounds were similar. At the end of six weeks, no unhealed wounds were present. Result of re-epithelization The mean time for 50% of re-epithelization was 21.4 days in the OZO group and 25.8 days in the SSD group (p<0.001). The mean time to 80% of re-epithelization was 25.4 days in the OZO group and 30.2 days in the SSD group (p<0.001). Re-epithelization of burn wounds was faster in Group OZO compared to Group SSD (Fig. 3). Wound colonization The scores of wound colonization were lower in Group O than in Group S within all weeks. However, these differences were significant only at weeks 2, 3, 4, and 6 (p<0.05) (Fig. 4). Thickness of epidermis The mean thickness of the epidermis was 0.12 mm in Group OZO and 0.16 mm in Group SSD (p<0.001). 379


Ulus Travma Acil Cerrahi Derg

(a)

(b)

(c)

Fig. 6. (a) Histopathologic appearance of normal epidermis; (b) histopathologic appearance of epidermis of a rabbit treated by OZO; c: histopathologic appearance of epidermis of a rabbit treated by SSD. (OZO: Zinc oxide, SSD: Silver sulfadiazine)

OZO, and of dermis from a rabbit treated with SSD are presented in Figures 8a, b and c, respectively.

Dermis

5 4.5 4

Thickness of scar tissue

(mm)

3.5 3 2.5 2 1.5 1 0.5 0

Zinc oxide

Silver sulfadiazine

Fig. 7. Mean dermis thickness in both groups (mm).

These values were higher than normal values, indicating that epidermal maturation was better in Group OZO than Group SSD (Fig. 5). The histopathologic appearances of normal epidermis, of epidermis from a rabbit treated with OZO and of epidermis from a rabbit treated with SSD are presented in Figures 6a, 6b and 6c, respectively. Thickness of dermis In both groups, the histologically detected thicknesses of the dermis were higher than normal values (3.8 mm in Group OZO and 4.7 mm in Group SSD), and the difference was statistically significant (p<0.001) (Fig. 7). The histopathologic appearances of normal dermis, of dermis from a rabbit treated with

(a)

(b)

The mean thicknesses of scar tissue were 2.4 mm in Group OZO and 3.2 mm in Group SSD (p<0.001). The scar tissue was significantly thinner in Group OZO compared to Group SSD (Fig. 9). The histopathological appearances of scar tissue in rabbits treated with OZO and SSD are shown in Figures 10a and b, respectively.

DISCUSSION Burns are one of the most important health issues. Topical treatment is very important in the treatment of burns, and multiple agents have been used for this purpose. Some have been used for a long time; however, others have only recently appeared in the literature. An ideal topical agent should heal the wound in a shorter period with the best results, decrease the rates of mortality and morbidity by preventing bacterial contamination and sepsis, and be easily accessible and cheaper. As agents with such properties have yet to be identified or manufactured, studies to discover the ideal agent are ongoing. As the main part of the study, the effects of OZO on burn wounds were investigated, and the results were compared with those obtained with SSD. Recently, SSD has emerged as the most commonly used topical agent in burn wounds

(c)

Fig. 8. (a) Histopathologic appearance of normal dermis; (b) histopathologic appearance of dermis of a rabbit treated by OZO; (c) histopathologic appearance of dermis of a rabbit treated by SSD. (OZO: zinc oxide, SSD: silver sulfadiazine). 380

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Comparison of topical zinc oxide and silver sulfadiazine in burn wounds

3

(mm)

2.5 2 1.5 1 0.5 0

At the meeting of the World Union of Wound Healing Societies in Paris in 2004, zinc was accepted to have potential benefits in wound healing.[20] The defect of zinc-finger transcription factors in mRNA coding growth factors causes impaired wound healing. [25,26] In a rat burn model, it was reported that the zinc level increases to 15-20% at the margin of the wound in the first 24 hours, and the level reaches 30% when the epidermal proliferation and granulation tissue are at maximum level. The more the zinc level decreases, the more mitotic activity decreases, and then scar maturation occurs.[27-29] Topical application of zinc decreases the rate of debris and necrotic material and increases the epithelization.[30-33] According to Kietzmann,[35] locally applied zinc accelerates the healing of ulcerated skin. According to various randomized controlled studies, topical application of zinc has beneficial effects on leg ulcers, pressure ulcers and diabetic foot ulcers. [25,33,36-38] In light of these data, zinc may be suggested to be closely related to wound healing. However, no study has been reported or encountered in the literature about the effects of OZO on burn wounds. In several previous studies, zinc was used topically for both normal skin and open wounds; as a result of these studies, no systemic toxic effects were mentioned after the absorption.[27-30] Therefore, in our study, investigation of the systemic effects of zinc was considered to be unnecessary, consistent with previous studies. [22-24]

3.5

Zinc oxide

Silver sulfadiazine

Fig. 9. Mean scar tissue thickness in both groups (mm).

due to its antimicrobial effects.[1] Silver contained resolved by SSD has a preventive effect by terminating most of the microorganisms, even fungi.[2] It also accelerates the wound healing process through the inhibition of matrix metalloproteinases and increases the epithelization.[3-8] Studies opposed to SSD can also be found in the literature. In a study by Maghsoudi et al.,[9] wet gauze dressings were reported to give better results than SSD in the treatment of burn wounds. The same study showed that SSD delays wound healing. Likewise, in a randomized controlled study by Khorasani et al.[10] comparing aloe vera with SSD, it was concluded that wound healing was better in the aloe vera group and that SSD delays re-epithelization in burn wounds. SSD was also determined to delay the separation of scar tissue in deep wounds. [10-14] Hypertrophic and atrophic scar formation can be seen in the treatment of SSD, especially in processes longer than three weeks.[15,16] It was also reported that renal toxicity resolves after the treatment with SSD is discontinued.[17] SSD may cause transient leukopenia, probably due to bone marrow toxicity.[18] In the light of such data, it may be suggested that SSD is not an ideal topical agent in the treatment of burn wounds. The significance of zinc has been known in medical science since ancient times.[19-21] Recent data show that zinc is found in more than 300 enzymes in the human body and also has preventive effects against infections.

(a)

In order to determine the effects of zinc on burn wounds, OZO was used in a rabbit burn model, and the effects of zinc were compared to those obtained from the use of SSD. In Group OZO, the times when 50% and 80% of re-epithelization were observed were found to be 4 and 5 days shorter, respectively (p<0.001). The period ranging from one to four days is very important in the treatment of burn wounds with zinc in human and animal wounds.[39-41] As a result, a four- or five-day healing period gained through the treatment of OZO makes it more advantageous compared to SSD.

(b)

Fig. 10. (a) Histopathological appearance of scar tissue of a rabbit treated by OZO, (b) histopathological appearance of scar tissue of a rabbit treated by SSD. (OZO: zinc oxide, SSD: silver sulfadiazine) Cilt - Vol. 18 Say覺 - No. 5

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The score of wound colonization was lower in Group OZO than in Group SSD at all weeks. However, this difference was only significant at weeks 2, 3, 4, and 6 (p<0.005). This parameter may be suggested to show the superiority of OZO in the treatment of burn wounds. Another criterion of burn wound healing determined in the present study was the thickness of the epidermis, dermis and scar tissues. The thicknesses of epidermis and dermis measured histopathologically were higher in both groups compared to normal values. The mean thickness of the epidermis was 0.12 mm in Group OZO and 0.16 mm in Group SSD (p<0.001). The mean thickness of the dermis was also lower in Group OZO than Group SSD (p<0.001). Likewise, the mean thickness of scar tissue was lower in Group OZO compared to Group SSD (p<0.001). In this study, the duration to re-epithelization, scale of wound colonization, and thicknesses of the epidermis, dermis and scar tissues were used to assess the process of burn wound healing. Given all these parameters, OZO was determined to be superior to SSD in the treatment of partial-thickness burn wounds. Considering the adverse effects of SSD, the superiority of OZO became more prominent. As no burn study related to the use of topical zinc is available at present, our results could not be compared to the literature. Therefore, further experimental and clinical studies regarding the effects of zinc oxide on burn wounds are needed to provide better results for medical science. Our study concluded that partial-thickness burns may be treated with OZO, and newer studies should address these issues for application in humans. In conclusion, in an experimental burn model, zinc oxide was indicated to be superior to SSD when used topically. Clinicians should be aware of the beneficial effects of zinc oxide in the treatment of burn wounds.

REFERENCES 1. Papini RP, Wilson AP, Steer JA, McGrouther DA, Parkhouse N. Wound management in burn centres in the United Kingdom. Br J Surg 1995;82:505-9. 2. Vloemans AF, Soesman AM, Suijker M, Kreis RW, Middelkoop E. A randomised clinical trial comparing a hydrocolloid-derived dressing and glycerol preserved allograft skin in the management of partial thickness burns. Burns 2003;29:702-10. 3. Gilman & Goodman. Pharmacologic basis of therapeutics. 5th ed. New York: McMullin; 1975. p. 930. 4. Warriner R, Burrell R. Infection and the chronic wound: a focus on silver. Adv Skin Wound Care 2005;18:2-12. 5. Atiyeh BS, Costagliola M, Hayek SN, Dibo SA. Effect of silver on burn wound infection control and healing: review of the literature. Burns 2007;33:139-48. 6. Wright JB, Lam K, Buret AG, Olson ME, Burrell RE. Early healing events in a porcine model of contaminated wounds: effects of nanocrystalline silver on matrix metalloproteinases, cell apoptosis, and healing. Wound Repair Regen 382

2002;10:141-51. 7. Demling RH, Leslie DeSanti MD. The rate of re-epithelialization across meshed skin grafts is increased with exposure to silver. Burns 2002;28:264-6. 8. Lansdown AB. Silver. 2: Toxicity in mammals and how its products aid wound repair. J Wound Care 2002;11:173-7. 9. Maghsoudi H, Monshizadeh S, Mesgari M. A comparative study of the burn wound healing properties of salinesoaked dressing and silver sulfadiazine in rats. Indian J Surg 2011;73:24-7. 10. Khorasani G, Hosseinimehr SJ, Azadbakht M, Zamani A, Mahdavi MR. Aloe versus silver sulfadiazine creams for second-degree burns: a randomized controlled study. Surg Today 2009;39:587-91. 11. Cho Lee AR, Leem H, Lee J, Park KC. Reversal of silver sulfadiazine-impaired wound healing by epidermal growth factor. Biomaterials 2005;26:4670-6. 12. Poon VK, Burd A. In vitro cytotoxity of silver: implication for clinical wound care. Burns 2004;30:140-7. 13. Hollinger MA. Toxicological aspects of topical silver pharmaceuticals. Crit Rev Toxicol 1996;26:255-60. 14. Sawhney CP, Sharma RK, Rao KR, Kaushish R. Long-term experience with 1 per cent topical silver sulphadiazine cream in the management of burn wounds. Burns 1989;15:403-6. 15. Sheridan RL, Petras L, Lydon M, Salvo PM. Once-daily wound cleansing and dressing change: efficacy and cost. J Burn Care Rehabil 1997;18:139-40. 16. Klasen HJ. A historical review of the use of silver in the treatment of burns. II. Renewed interest for silver. Burns 2000;26:131-8. 17. Dickinson SJ. Topical therapy of burns in children with silver sulfadiazine. N Y State J Med 1973;73:2045-9. 18. Chaby G, Viseux V, Poulain JF, De Cagny B, Denoeux JP, Lok C. Topical silver sulfadiazine-induced acute renal failure. [Article in French] Ann Dermatol Venereol 2005;132:891-3. [Abstract] 19. Choban PS, Marshall WJ. Leukopenia secondary to silver sulfadiazine: frequency, characteristics and clinical consequences. Am Surg 1987;53:515-7. 20. Lansdown AB, Mirastschijski U, Stubbs N, Scanlon E, Agren MS. Zinc in wound healing: theoretical, experimental, and clinical aspects. Wound Repair Regen 2007;15:2-16. 21. Prasad AS. Zinc: an overview. Nutrition 1995;11:93-9. 22. Jones PW, Williams DR. The use and role of zinc and its compounds in wound healing. Met Ions Biol Syst 2004;41:13983. 23. O’Dell BL. Zinc plays both structural and catalytic roles in metalloproteins. Nutr Rev 1992;50:48-50. 24. Vallee BL, Falchuk KH. The biochemical basis of zinc physiology. Physiol Rev 1993;73:79-118. 25. Agren MS, Ostenfeld U, Kallehave F, Gong Y, Raffn K, Crawford ME, et al. A randomized, double-blind, placebocontrolled multicenter trial evaluating topical zinc oxide for acute open wounds following pilonidal disease excision. Wound Repair Regen 2006;14:526-35. 26. Sum EY, O’Reilly LA, Jonas N, Lindeman GJ, Visvader JE. The LIM domain protein Lmo4 is highly expressed in proliferating mouse epithelial tissues. J Histochem Cytochem 2005;53:475-86. 27. Zhu CH, Ying DJ, Mi JH, Zhang W, Dong SW, Sun JS, et al. The zinc finger protein A20 protects endothelial cells from burns serum injury. Burns 2004;30:127-33. 28. Lansdown AB, Sampson B, Rowe A. Sequential changes in Eylül - September 2012


Comparison of topical zinc oxide and silver sulfadiazine in burn wounds

trace metal, metallothionein and calmodulin concentrations in healing skin wounds. J Anat 1999;195:375-86. 29. Savlov ED, Strain WH, Huegin F. Radiozinc studies in experimental wound healing. J Surg Res 1962;2:209-12. 30. Agren MS, Franzén L. Influence of zinc deficiency on breaking strength of 3-week-old skin incisions in the rat. Acta Chir Scand 1990;156:667-70. 31. Keefer KA, Iocono JA, Ehrlich HP. Zinc-containing wound dressings encourage autolytic debridement of dermal burns. Wounds 1998;10:54-8. 32. Lansdown AB. Influence of zinc oxide in the closure of open skin wounds. Int J Cosmet Sci 1993;15:83-5. 33. Apelqvist J, Larsson J, Stenström A. Topical treatment of necrotic foot ulcers in diabetic patients: a comparative trial of DuoDerm and MeZinc. Br J Dermatol 1990;123:787-92. 34. Gang RK. Adhesive zinc tape in burns: results of a clinical trial. Burns 1980;7:322-5. 35. Kietzmann M. Improvement and retardation of wound healing: effects of pharmacological agents in laboratory animals.

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Vet Dermatol 1999;10:83-8. 36. Agren MS, Strömberg HE. Topical treatment of pressure ulcers. A randomized comparative trial of Varidase and zinc oxide. Scand J Plast Reconstr Surg 1985;19:97-100. 37. Brandrup F, Menné T, Agren MS, Strömberg HE, Holst R, Frisén M. A randomized trial of two occlusive dressings in the treatment of leg ulcers. Acta Derm Venereol 1990;70:2315. 38. Strömberg HE, Agren MS. Topical zinc oxide treatment improves arterial and venous leg ulcers. Br J Dermatol 1984;111:461-8. 39. Greenhalgh DG. Wound healing. In: Herndon DN, editor. Total burn care. London: W.B. Saunders; 2002. p 523-95. 40. Fu X, Li X, Cheng B, Chen W, Sheng Z. Engineered growth factors and cutaneous wound healing: success and possible questions in the past 10 years. Wound Repair Regen 2005;13:122-30. 41. Singer AJ, Clark RA. Cutaneous wound healing. N Engl J Med 1999;341:738-46.

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):384-388

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.58855

The value of serum fibrinogen level in the diagnosis of acute appendicitis Akut apandisit tanısında serum fibrinojen düzeyinin değeri Öner MENTEŞ,1 Mehmet ERYILMAZ,2 Ali HARLAK,1 Erkan ÖZTÜRK,1 Turgut TUFAN1

BACKGROUND

AMAÇ

The aim of this study was to investigate the importance of serum fibrinogen level in the diagnosis of acute appendicitis.

Bu çalışmada akut apandisit tanısında serum fibrinojen düzeyinin önemi araştırıldı.

METHODS

GEREÇ VE YÖNTEM

This study was performed on 201 patients who admitted to our clinic. Symptoms, signs, duration of symptoms, and laboratory indicators of appendicitis were recorded, in keeping with the Alvarado score for acute appendicitis. The ultimate diagnosis was based on histopathological results. Serum fibrinogen levels were detected before surgery. The sensitivity, specificity, and predictive values of single test and test combinations were calculated at different cut-off levels. RESULTS

Kliniğimize başvuran 201 hasta çalışmaya alındı. Hastaların semptomları, semptom süreleri, muayene bulguları, laboratuvar bulguları ve akut apandisit için Alvarado skorları kaydedildi. Kesin tanı histopatolojik inceleme ile konuldu. Ameliyat öncesi kan fibrinojen değerine bakıldı. Tek bir testin ve test kombinasyonlarının duyarlılık, özgüllük ve öngörü değeri farklı seviyelerinde hesaplandı. BULGULAR

During the study period, 201 patients underwent surgery for suspected acute appendicitis. Appendicitis was confirmed in 179 (89%) patients. The mean age was 24.8±7.7 (range, 20-57) years, and 154 (76.6%) patients were male and 47 (23.4%) female. The best diagnostic cut-off point for fibrinogen was found at 245.5 mg/dl, for white blood cells (WBC) at 11,900x109/L and for Alvarado score at 7.

Çalışma süresinde 201 hasta akut apandisit ön tanısı ile ameliyat edildi. Histopatolojik inceleme sonrası 179 (%89) hasta akut apandisit tanısı aldı. Hastaların yaş ortalaması 24,8±7,7 (dağılım 20-57) yıldı, 154 (%76.6) hasta erkek, 47 (23.4%) hasta kadındı. Akut apandisit tanısı için kesim değeri fibrinojen için 245,5 mg/dl, beyaz küre sayımı için 11.900x109/L ve Alvarado skoru için 7 olarak bulundu.

CONCLUSION

SONUÇ

The use of fibrinogen blood level may be a new diagnostic acute-phase reactant in the diagnosis of acute appendicitis. The formulation of a triple test is recommended as criteria in deciding emergency surgery or observation.

Akut apandisit tanısında fibrinojenin serum değeri yeni bir akut faz reaktamı olarak kullanılabilir. Üçlü test formülünün kullanılması gözlem veya acil cerrahi kararını vermede yardımcı olabileceği düşünülmektedir.

Key Words: Acute appendicitis; fibrinogen; diagnosis.

Anahtar Sözcükler: Akut apandisit; fibrinojen; tanı.

Acute appendicitis (AA) is the most common indication for emergent surgery and affects a wide range of patients at any age. Approximately 7% of the popu-

lation will develop appendicitis at some time during their lives.[1,2] The aim of the clinical evaluation of patients with suspected AA is primarily performed in

Depertments of 1General Surgery, 2Emergency Medicine, Gulhane Military Medical Faculty, Ankara, Turkey.

Gülhane Askeri Tıp Akademisi, 1Genel Cerrahi Anabilim Dalı, 2 Acil Cerrahi Anabilim Dalı, Ankara.

Correspondence (İletişim): Öner Menteş, M.D. Gülhane Askeri Tıp Akademisi, Genel Cerrahi Anabilim Dalı, Etlik 06018 Ankara, Turkey. Tel: +90 - 312 - 304 50 15 e-mail (e-posta): onermentes@yahoo.com

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Serum fibrinogen levels in acute appendicitis

Various imaging modalities, biochemical markers, and scoring systems have been introduced, with a view to lower the negative appendectomy rate. However, there is continuing controversy about their routine use, while studies are ongoing to investigate how to improve the diagnostic accuracy in AA.[6] In the past, studies have discussed the high incidence of negative appendectomy as a way of preventing perforation of the appendix. It was assumed that the morbidity associated with a negative appendectomy was not severe enough to allow the risk of appendiceal perforation. This aspect was challenged by Flum et al.,[7] who showed that patients who underwent negative appendectomy were also observed to have more comorbidities, longer length of hospital stay, and higher infection and case fatality rates. This and other studies have described the significant burden of negative appendectomy and have aimed to identify better diagnostic tests in the management of AA. The aim of this study was to determine the predictive value of serum fibrinogen level in indicating appendectomy immediately.

MATERIALS AND METHODS This study was performed on 201 patients who admitted to our clinic between March 2005 and May 2007 with suspected AA. Patient demographics and presenting signs and symptoms were documented. The patients’ symptoms, signs, duration of symptoms, and laboratory indicators were recorded, in keeping with the Alvarado score for appendicitis.[8] Based on these findings, Alvarado score was calculated for each patient. Patient symptoms included nausea, vomiting, migratory pain, anorexia, right lower quadrant pain, body temperature >37.3°C, and white blood cell (WBC) count, left shift on differential. The WBC count was determined by a technical hematological cell counter (Beckman-Coulter, Krefeld), and the upper limit was defined as 10.0x109/L. All removed appendixes were examined by a routine protocol in which the ultimate diagnosis was based on histopathological results. Blood samples for determining fibrinogen serum levels were collected before the surgical procedure and measured by the clotting assay of Clauss method. The upper normal limit was defined as 400 mg/dl. The sensitivity, specificity, and predictive values of single Cilt - Vol. 18 Sayı - No. 5

test and test combinations were calculated at different cut-off levels. The decision to operate was the prerogative of the surgeon based on overall clinical judgment. Statistical Analysis The non-parametric Kruskal-Wallis test was used for multiple group comparisons. In case of significance, individual differences were identified with the Mann-Whitney U test. All p values of <0.05 were considered as statistically significant. Receiver operating characteristic (ROC) curves and the related areas under the curve (AUC) were calculated. Tests for significance of AUC to be >0.5, calculation of 95% confidence limits of the AUC and comparison of ROC curves were done.

RESULTS During the study period, 201 patients underwent surgery for suspected AA. Appendicitis was confirmed in 179 (89%) patients. The mean age was 24.8±7.7 (range, 20-57) years, and 154 (76.6%) patients were male and 47 (23.4%) female. To investigate the diagnostic value of fibrinogen, WBC, and Alvarado score, ROC curves were calculated. For the diagnosis of appendicitis, the best cut-off point for fibrinogen was found at 245.5 mg/dl, for WBC at 11,900, and for Alvarado score at 7 (Fig. 1). Predictive value, sensitivity, specificity, and accuracy of combined tests in the diagnosis of AA are shown in Table 1. Distribution of fibrinogen blood level, WBC and Alvarado score according to the final pathology are shown in Table 2. According to the cut-off levels, risk factors were derived from an unconditional logistic regression

1.0

Fibrinogen WBC Alvarado Reference line

0.8 Sensitivity

order to avoid appendiceal perforation and subsequent complications, while minimizing the number of unnecessary laparotomies.[3] The goal of modern surgical management is essentially the same and focuses on a balance between the rate of false-negative laparotomy and the rate of perforation at the time of surgical exploration.[4,5]

0.6

0.4

0.2

0.0 0.0

0.2

0.4

0.6

0.8

1.0

1-Specificity

Fig. 1. ROC curve for fibrinogen blood level, WBC, and Alvarado score. 385


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Table 1. Predictive value, sensitivity, specificity, and accuracy of combined tests in the diagnosis of acute appendicitis

95% CI for OR

Tests

Fibrinogen >245.5 mg/dl WBC >11.900/L Alvarado score >7 Fibrinogen >245.5 mg/dl WBC >11.900 /L Fibrinogen >245.5 mg/dl Alvarado score >7 Alvarado >7 WBC >11.900 /L Fibrinogen >245.5 mg/dl Alvarado score >7 WBC >11.900 /L

PPV

NPV

Sensitivity (%)

Specificity (%)

Accuracy (%)

OR

Lower

Upper

91.97 96.24 96.43

17.18 25.0 20.22

70.39 71.51 60.34

50.0 77.27 81.82

68.16 72.14 62.69

2.38 8.53 6.85

0.97 2.99 2.22

5.82 24.35 21.06

96.81

36.0

85.05

75.0

84.03

17.06

4.16

69.92

94.77

29.03

77.78

81.81

78.18

15.75

3.17

78.30

96.94

29.63

71.42

84.21

73.02

13.33

3.67

48.4

98.55

42.86

85.0

90.0

86.0

51.0

5.91

440.11

analysis. According to the model, the probability of AA for an individual patient can be calculated as: 1/1+2.66-y y= -2.8066 + (0.0076 x fibrinogen blood level) + (0.5094 x Alvarado score) + (0.000035 x WBC) – (0.7082 x duration of symptoms [<24 h (1); ≥24 h (0)]). The score had a minimum of zero and maximum of one point. The cut-off level for AA is ≥0.75. Over this level, we can estimate the real AA case in over 92.18%. If the score was <0.75, the possibility of appendicitis was less and the patient should be kept under observation. When the score reaches ≥0.75, the patient should be taken for surgery.

DISCUSSION The aim of this study was to evaluate the value of the serum fibrinogen level in the diagnosis of suspected AA and to determine the relationship between the Alvarado score and WBC. Many attempts have been made to determine ways of decreasing the negative laparotomy rate in clinically suspected AA. It would be very important to differentiate early appendicitis from non-specific abdominal pain. However, a carefully detailed history, physical examination, and standard laboratory studies do not always clearly detect early AA. Furthermore, delays in diagnosis can be harmful and may convert a relatively uncomplicated case to substantial morbidity or even mortality in patients with comorbid illnesses.

Table 2. Distribution of fibrinogen blood level, WBC, and Alvarado score according to the final pathology Diagnosis (according to final pathology)

Normal appendix Simple acute appendicitis Gangrenous appendix Perforated appendix

Fibrinogen blood level* (mg/dl) Mean ±SDΔ (range, - )

White blood cell* Mean ±SDΔ (range, - )

Alvarado score* Mean±SDΔ (range, -)

≤245.5

>245.5

≤11.900/L

>11.900/L

<7

9

13

18

4

15

7

200.3±37.22

327±56.63

9030±1682.07

16.100±1186.03

4.8±1.08

7.75±0.88

(range, 3-6)

(range, 7-9)

(range, 122-245) (range, 246-449)

(range, 9100-11,800) (range, 15,200-17,700)

≥7

24

60

25

59

22

62

206.82±32.06

339±71.64

9487.5±2172.22

15.160±2350.23

5.04±084

8.16±1.05

(range, 111-245) (range, 246-505)

(range, 3900-11.800) (range, 12.000-21.300)

(range, 3-6) (range, 7-10)

19

43

14

48

9

53

219.15±20.35

362.95±79.75

9542.85±2145.01

16.229.16±3118.8

4.8±1.16

8.3±0.76

(range, 160-245) (range, 251-596) 8

25

215.25±25.7

37.4±83.84

(range, 170-245) (range, 250-605)

(range, 4600-11,600) (range, 12,000-24,400) 3

30

10.600±608.27

14.900±2208.65

(range, 9900-10,900) (range, 12,000-21,300)

(range, 3-6) (range, 7-10) 2

31

5.5±0.5

8.29±0.9

(range, 5-6) (range, 7-10)

*Cut-off levels of parameters, Δ Standard deviation.

386

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Serum fibrinogen levels in acute appendicitis

The optimal test should combine a high sensitivity with a high predictive value of a negative result. When using the test’s standard reference interval, the manual determination of bands showed a significantly lower sensitivity compared with the other tests. Further, the diagnostic accuracy of a test may be improved by changing the cut-off level if the test result is considered positive. If the cut-off level is elevated, the sensitivity or number of true-positive patients detected by the test will decrease, while the specificity or number of true-negative patients will increase. The exact value of the test is determined by ROC calculation. We determined the exact value for WBC, Alvarado score and fibrinogen blood level by ROC calculation. The WBC count is the test probably used most often to support the diagnosis of AA. However, WBC is a non-specific reaction induced by many different causes like physical stress, acute or chronic inflammation and several other conditions. In patients with AA, WBC show an average elevation to approximately 15.0x109/L.[9] Pieper and colleagues[10] reported experience with 493 patients of whom only 67% had WBC greater than 11.0x109/L. Cardall and colleagues[11] found the sensitivity of WBC as 76%, specificity as 52%, positive predictive value (PPV) as 42%, and negative predictive value (NPV) as 82%. In our study, the best cut-off point of WBC for early diagnosis of AA was found as 11,900x109/L, and at this point, the sensitivity, specificity, PPV, NPV, and accuracy were calculated as 72%, 77%, 96%, 25%, and 72%, respectively. In this respect, it can be said that if the WBC level is accepted as over 11,900x109/L, its diagnostic value will be more reliable in the diagnosis of AA. In addition, we determined the probability of AA to be 8.53 times more when WBC is over 11,900x109/L. Diagnostic scores for AA have been claimed to lower the non-therapeutic operation rate. The Alvarado scoring system is a point scoring system for the diagnosis of appendicitis based on clinical science and symptoms and a differential WBC. The accuracy of the Alvarado score in a clinical preoperative diagnosis of AA has been reported as ranging from 50% to 95%.[9,10] In his original paper, Alvarado recommends surgery for all patients with a score of 7 or more and observation for patients with scores of 5 or 6.[8] In our study, the best cut-off point of the Alvarado score for early diagnosis of AA was found as 7, and at this point, sensitivity, specificity, PPV, NPV, and accuracy were calculated at 60%, 82%, 96%, 20%, and 63%, respectively. According to our study results, probability of AA was found to be 6.85 times more when the Alvarado score was over 7. Plasma fibrinogen is an acute phase protein and therefore probably Cilt - Vol. 18 Sayı - No. 5

increases with inflammation or tissue necrosis. Interpretation of raised fibrinogen may be complicated by its behavior as an acute-phase reactant. For example, plasma fibrinogen concentrations are raised after acute stroke and acute myocardial infarction.[12] Among all known thrombin substrates, fibrinogen stands out as a central factor in hemostasis and a contributor to the inflammatory response.[13] Fibrinogen deposition is a universal feature in injured tissues and inflammatory foci. In vitro studies have shown that fibrinogen can profoundly alter WBC function, leading to changes in cell migration, phagocytosis, production of chemokines and cytokines, degranulation, and other processes. Many of the effects of fibrinogen on leukocyte activity appear to be mediated by a specific receptor on leukocytes, the integrin receptor αMβ2.[14,15] Leukocyte interaction with fibrinogen or its degradation products has special importance at sites of inflammation since fibrinogen may gain access to the extravascular compartment by exudation, where it encounters migrating leukocytes.[16] It is well known that both the extent of leukocyte recruitment and the proinflammatory action of the migrating leukocytes determine the intensity of an inflammatory reaction, and peripheral human neutrophils are capable of phagocytosis, spreading, and chemotaxis.[17-19] We aimed to investigate serum fibrinogen level as a new marker in the diagnosis of AA. Our study is probably the first report to use fibrinogen blood level in the diagnosis of AA. In our current study, the best cut-off for serum fibrinogen level was found as 245.5 mg/dl, and at this point, the sensitivity, specificity, PPV, NPV, and accuracy were calculated as 70%, 50%, 92%, 17%, and 68%, respectively. Probability of AA was found to be 2.38 times more when fibrinogen blood level was over 245.5 mg/dl. Fibrinogen results were found to have similar efficacy to WBC and Alvarado scores in the diagnosis of AA. Blood tests have been shown to have low sensitivity and specificity in differentiating simple AA from a perforated appendix in a majority of the studies. [20,21] However, in a few studies, the WBC was more sensitive than C-reactive protein (CRP) in the diagnosis of simple AA,[22] and CRP was reported as more sensitive than WBC in cases of a perforated appendix. [23]

Numerous studies have shown that increased CRP levels in the blood aid in the accurate diagnosis of AA. Han-ping Wu and colleagues[24] noticed that the mean CRP level in patients with perforated appendicitis was much greater than in patients with simple appendicitis, and they found the role of CRP did serve in the differential diagnosis of perforated appendicitis. That study 387


Ulus Travma Acil Cerrahi Derg

mentioned CRP levels using different cut-off values based on how long the patient’s symptoms were present to improve the diagnostic accuracy of simple and perforated appendicitis, and that CRP would be helpful in predicting appendicitis earlier and reducing the rate of complications caused by delay in diagnosis. In our study, we found the same results according to fibrinogen blood level and the duration of symptoms (<24 h or >24 h). Fibrinogen blood level and duration of symptoms have shown to contribute greatly to the diagnosis of AA. The diagnostic value of a single test in AA is limited because this process cannot be differentiated from other acute inflammatory conditions. The triple test combination’s sensitivity, specificity, PPV, NPV, and accuracy were calculated as 85%, 90%, 99%, 43%, and 86%, respectively. Probability of AA was found to be 51 times more when the triple test levels were over cut-off levels. In conclusion, AA remains the most common condition requiring emergent surgery. Early diagnosis plays a key role in preventing complications originating from perforation. However, surgeons must achieve a balance between premature operation with a high negative appendectomy rate and a delayed diagnosis (and surgery) with a higher perforation rate. There is no sign, symptom, or laboratory test that is 100% reliable in the diagnosis of AA. Our results suggest that the use of fibrinogen blood level may be a new diagnostic acute-phase reactant in the diagnosis of AA. The formulation of the triple test’s result is recommended as a guide in deciding which patient undergoes emergency surgery or observation. Acknowledgements Mr. Ahmet Gul made significant contributions to the study though his statistical analysis.

REFERENCES 1. Feldman M. The small intestine. In: Sleisenger M, Fordtran J, editors. Gastrointestinal and liver diseases. 6th ed. Philadelphia, PA: W.B. Saunders; 1998. p. 1778-87. 2. Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol 1990;132:910-25. 3. Dueholm S, Bagi P, Bud M. Laboratory aid in the diagnosis of acute appendicitis. A blinded, prospective trial concerning diagnostic value of leukocyte count, neutrophil differential count, and C-reactive protein. Dis Colon Rectum 1989;32:855-9. 4. Velanovich V, Satava R. Balancing the normal appendectomy rate with the perforated appendicitis rate: implications for quality assurance. Am Surg 1992;58:264-9. 5. Memon MA, Fitztgibbons RJ Jr. The role of minimal ac-

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cess surgery in the acute abdomen. Surg Clin North Am 1997;77:1333-53. 6. Ma KW, Chia NH, Yeung HW, Cheung MT. If not appendicitis, then what else can it be? A retrospective review of 1492 appendectomies. Hong Kong Med J 2010;16:12-7. 7. Flum DR, Koepsell T. The clinical and economic correlates of misdiagnosed appendicitis: nationwide analysis. Arch Surg 2002;137:799-804. 8. Alvarado A. A practical score for the early diagnosis of acute appendicitis. Ann Emerg Med 1986;15:557-64. 9. Ricci MA, Trevisani MF, Beck WC. Acute appendicitis. A 5-year review. Am Surg 1991;57:301-5. 10. Pieper R, Kager L, Näsman P. Acute appendicitis: a clinical study of 1018 cases of emergency appendectomy. Acta Chir Scand 1982;148:51-62. 11. Cardall T, Glasser J, Guss DA. Clinical value of the total white blood cell count and temperature in the evaluation of patients with suspected appendicitis. Acad Emerg Med 2004;11:1021-7. 12. Dormandy J, Ernst E, Matrai A, Flute PT. Hemorrheologic changes following acute myocardial infarction. Am Heart J 1982;104:1364-7. 13. Molmenti EP, Ziambaras T, Perlmutter DH. Evidence for an acute phase response in human intestinal epithelial cells. J Biol Chem 1993;268:14116-24. 14. Flick MJ, Du X, Witte DP, Jirousková M, Soloviev DA, Busuttil SJ, et al. Leukocyte engagement of fibrin(ogen) via the integrin receptor alphaMbeta2/Mac-1 is critical for host inflammatory response in vivo. J Clin Invest 2004;113:1596606. 15. Tang L, Eaton JW. Fibrin(ogen) mediates acute inflammatory responses to biomaterials. J Exp Med 1993;178:2147-56. 16. Sitrin RG, Pan PM, Srikanth S, Todd RF 3rd. Fibrinogen activates NF-kappa B transcription factors in mononuclear phagocytes. J Immunol 1998;161:1462-70. 17. Watson RW, Rotstein OD, Nathens AB, Parodo J, Marshall JC. Neutrophil apoptosis is modulated by endothelial transmigration and adhesion molecule engagement. J Immunol 1997;158:945-53. 18. Nathan C, Srimal S, Farber C, Sanchez E, Kabbash L, Asch A, et al. Cytokine-induced respiratory burst of human neutrophils: dependence on extracellular matrix proteins and CD11/CD18 integrins. J Cell Biol 1989;109:1341-9. 19. Rubel C, Fernández GC, Dran G, Bompadre MB, Isturiz MA, Palermo MS. Fibrinogen promotes neutrophil activation and delays apoptosis. J Immunol 2001;166:2002-10. 20. Rothrock SG, Pagane J. Acute appendicitis in children: emergency department diagnosis and management. Ann Emerg Med 2000;36:39-51. 21. Andersson RE. Meta-analysis of the clinical and laboratory diagnosis of appendicitis. Br J Surg 2004;91:28-37. 22. Grönroos JM, Grönroos P. Leucocyte count and C-reactive protein in the diagnosis of acute appendicitis. Br J Surg 1999;86:501-4. 23. Rodríguez-Sanjuán JC, Martín-Parra JI, Seco I, García-Castrillo L, Naranjo A. C-reactive protein and leukocyte count in the diagnosis of acute appendicitis in children. Dis Colon Rectum 1999;42:1325-9. 24. Wu HP, Lin CY, Chang CF, Chang YJ, Huang CY. Predictive value of C-reactive protein at different cutoff levels in acute appendicitis. Am J Emerg Med 2005;23:449-53.

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):389-396

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.48827

Incarcerated abdominal wall hernia surgery: relationship between risk factors and morbidity and mortality rates (a single center emergency surgery experience) Boğulmuş abdominal duvar herni cerrahisi: Morbidite ve mortalite insidansının risk faktörleriyle ilişkisinin analizi (Tek merkezli acil cerrahi deneyimi) Erkan ÖZKAN, Mehmet Kamil YILDIZ, Tuğrul ÇAKIR, Ender DULUNDU, Cengiz ERİŞ, Mehmet Mahir FERSAHOĞLU, Ümit TOPALOĞLU BACKGROUND

AMAÇ

The aim of the present study was to investigate morbidityand mortality-related risk factors in patients undergoing surgery due to incarcerated abdominal wall hernia.

Bu çalışmada, acil cerrahi kliniğimizde boğulmuş abdominal duvar hernisi nedeniyle ameliyat edilen hastalarda morbidite ve mortaliteyle ilişkili risk faktörlerinin insidansı araştırıldı.

METHODS

The patients were grouped according to the type of hernia (inguinal, umbilical, incisional, femoral), and these groups were evaluated in terms of risk factors affecting morbidity and mortality such as age, gender, American Society of Anesthesiologists (ASA) score, type of anesthesia, concomitant diseases, and the presences of intestinal strangulation and necrosis.

GEREÇ VE YÖNTEM

RESULTS

BULGULAR

Inguinal hernia was frequent in males, whereas femoral hernia was frequent in females (p<0.001). The rate of intestinal resection due to strangulation and necrosis was found significantly higher among femoral hernias as compared to the other types of hernia (p<0.005 and p<0.001, respectively). Advanced age (≥65 years), concomitant disease, strangulation, necrosis, high ASA score (III-IV), time from the onset of symptoms, and time to hospital admission were found to have significant influences on morbidity and mortality. General anesthesia was found to be a risk factor for morbidity as well (p<0.05). CONCLUSION

Hastalar hem fıtık türüne göre (inguinal, umblikal, insizyonel, femoral) kendi aralarında hem de morbidite ve mortalite üzerine etkili faktörler bakımından; yaş, cinsiyet, Amerikan Anesteziyoloji Derneği (AAD) skoru, anestezi tipi, eşlik eden hastalıklar, intestinal boğulma ve nekroz varlığı gibi verilerle değerlendirildi.

İnguinal herni erkeklerde, umblikal ve femoral herni kadınlarda sıktı (p<0,001). Femoral hernide boğulma ve nekrozdan dolayı intestinal rezeksiyon diğer fıtık türlerine göre anlamlı olarak yüksek saptandı (sırasıyla, p<0,005 ve p<0,001). Morbidite ve mortalite üzerine; ileri yaş (≥65 yaş), ek hastalık, strangülasyon, nekroz, yüksek AAD skoru (III, IV), semptomların başlama ve hastaneye başvuru süresinin anlamlı etkisi bulundu. Genel anestezinin de morbidite için risk oluşturduğu görüldü (p<0,05). SONUÇ

Incarcerated abdominal wall hernias are surgical problems with high morbidity and mortality rates. Therefore, surgery should be planned under elective conditions when hernia is detected.

Boğulmuş abdominal duvar hernileri yüksek morbidite ve mortalite oranına sahip bir cerrahi problemdir. Bu yüzden herni saptandığında elektif koşullarda ameliyat planlanmalıdır.

Key Words: Abdominal wall hernia; incarceration; necrosis; strangulation.

Anahtar Sözcükler: Abdominal duvar hernisi; inkarserasyon; nekroz; strangülasyon.

5th Department of General Surgery, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey.

Haydarpaşa Numune Eğitim ve Araştırma Hastanesi, 5. Genel Cerrahi Kliniği, İstanbul.

Correspondence (İletişim): Erkan Özkan, M.D. Bosna Bulvarı, Taşlıbayır Sok. No: 28 B Blok Kat: 3 Da: 7, Üsküdar, İstanbul, Turkey. Tel: +90 - 216 - 542 32 32 e-mail (e-posta): dr.erkan@mynet.com

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Abdominal wall hernia (AWH) surgery is among the most frequently performed general surgical operations throughout the world.[1] Incarceration and strangulation are the most severe complications and account for a substantial portion of the patients presenting to emergency surgery clinics with acute abdominal complaints. Of the AWH cases, approximately 5%-13% may require emergency surgery due to incarceration and obstruction, and of the cases undergoing emergency surgery, 10%-15% may require intestinal resection due to necrosis.[2,3] In such surgical operations, inadequate preoperative preparation and the advanced age of the majority of the patients lead to a remarkable increase in morbidity and mortality.[4] The aim of the present study was to evaluate the rate of morbidity- and mortality-related risk factors in patients undergoing surgical operation in our emergency surgery clinic due to incarcerated AWH.

MATERIALS AND METHODS One hundred and ninety patients underwent emergency surgery due to incarcerated AWH in the 5th General Surgery Clinic of Haydarpasa Training and Research Hospital between December 2003 and January 2011. Indications for emergency surgery included irreducible mass, pain localized to the abdominal wall, and the signs and symptoms of mechanical intestinal obstruction. All patients were systematically evaluated prior to the operation. Complete blood count, biochemical analysis, and electrocardiography (ECG) were performed. Chest and direct abdominal radiographs were obtained while the patient was in a standing position. Those with a concomitant disease were preoperatively referred to the related clinics for consultation according to pathological data and medical histories. A single dose of second-generation cephalosporin was administered as prophylaxis. Cases with intestinal necrosis, which failed to normalize despite hot saline application and waiting after the release of the neck of the hernia sac, required resection and anastomosis. In patients with intestinal necrosis, antibiotherapy was continued in the postoperative period for an additional five days on average. All the patients underwent surgical operation within the first 24 hours of their hospital admission. General anesthesia was preferred for incarcerated umbilical hernia and incisional hernia of the upper abdomen, whereas spinal or general anesthesia was performed for incarcerated inguinal and femoral hernias and incisional hernia of the lower abdomen. The anesthesiologist decided the type of anesthesia to be performed. Inguinal incisions were used for inguinal and femoral hernias. However, the operation was completed by converting the incision into superior and inferior umbilical incision in inguinal and femoral hernia cases undergoing intestinal resection and anastomosis. Cooper’s ligament 390

hernioplasty (McWay) and anterior prosthetic meshplug hernioplasty methods were used in femoral hernia cases, whereas tension-free hernia repair was performed with monofilament polypropylene mesh in the other types of hernia. The term morbidity was used for postoperative major and minor complications (wound site, pulmonary and cardiac complications). The term mortality was used for deaths within 30 days of the operation or before discharge from the hospital. The patients were grouped according to the hernia type, and the groups were then evaluated with respect to the factors affecting morbidity and mortality, such as age, gender, American Society of Anesthesiologists (ASA) score, type of anesthesia, intestinal strangulation and necrosis, and the presence of a concomitant disease. Statistical analyses of the data were performed using Number Cruncher Statistical System (NCSS) 2007 and Power Analysis and Sample Size (PASS) 2008 Statistical Software (Utah, USA) program. In addition to the descriptive statistical methods (mean, standard deviation, ratio), Kruskal-Wallis test was used for the intergroup comparison of the quantitative data, whereas Mann-Whitney U-test was used to identify the group that caused the difference and for the comparison of two groups. Qualitative data were compared using chi-square test and Fisher’s exact test. A p value <0.05 was considered statistically significant.

RESULTS Of the 2,380 AWH cases (inguinal, umbilical, incisional, femoral) operated in the 5th General Surgery Clinic of Istanbul Haydarpasa Training and Research Hospital between December 2003 and January 2011, 190 (7.98%) underwent emergency surgery due to incarceration. Considering the hernia type, the rate of emergency surgery was the highest among femoral hernias (47.1%), but the lowest among inguinal hernias (6.1%) (Table 1). Of the emergency cases with incarceration, 55.8% had inguinal, 21.1% had umbilical, 14.7% had incisional, and 8.4% had femoral hernias. The mean age of the cases was 60.81±15.51 (range, 27-92 years). Of the cases, 64.7% (n=123) were males and 35.3% (n=67) were females. Table 1. The prevalence of emergency surgical procedures according to the hernia type Type of hernia Inguinal Umbilical Incisional Femoral

Emergency surgical procedure n (%)

Total surgical procedures n

106 (6.12%) 40 (9.95%) 28 (13.2%) 16 (47.05%)

1732 402 212 34

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Incarcerated abdominal wall hernia surgery

Table 2. Evaluations according to the hernia types

Type of hernia

Inguinal (n=106)

Age <65 64 (60.4%) ≼65 42 (39.6%) Gender Male 90 (84.9%) Female 16 (15.1%) American Society of Anesthesiologists I 6 (5.7%) II 42 (39.6%) III 46 (43.4%) IV 12 (11.3%) Anesthesia General 58 (54.7%) Spinal 48 (45.3%) Intestinal strangulation Positive 44 (41.5%) Negative 62 (58.5%) Concomitant disease Positive 51 (49.2%) Negative 55 (51.8%) Intestinal necrosis Positive 14 (13.2%) Negative 92 (86.8%) Morbidity Positive 14 (13.2%) Negative 92 (86.8%) Mortality Positive 5 (4.7%) Negative 101 (95.3%) Recurrence Yes 6 (5.9%) No 95 (94.1%)

Incisional (n=28)

Umbilical (n=40)

Femoral (n=16)

p

12 (42.9%) 16 (57.1%)

25 (62.5%) 15 (37.5%)

8 (50%) 8 (50%)

0.309

16 (57.1%) 12 (42.9%)

12 (30%) 28 (70%)

5 (31.3%) 11 (68.8%)

0.001**

2 (7.1%) 15 (53.6%) 3 (10.7%) 8 (28.6%)

6 (15%) 16 (40%) 12 (30%) 6 (15%)

0 (0%) 8 (50%) 4 (25%) 4 (25%)

0.026*

24 (85.7%) 4 (14.3%)

40 (100%) 0 (0%)

13 (81.3%) 3 (18.7%)

0.001**

16 (57.1%) 12 (42.9%)

18 (45%) 22 (55%)

14 (87.5%) 2 (12.5%)

0.005**

12 (42.8%) 16 (57.2%)

17 (42.5%) 23 (57.5%)

7 (43.7%) 9 (56.3%)

0.913

7 (25%) 21 (75%)

6 (15%) 34 (85%)

10 (62.5%) 6 (37.5%)

0.001**

7 (25%) 21 (75%)

4 (10%) 36 (90%)

2 (12.5%) 14 (87.5%)

0.336

1 (3.6%) 27 (96.4%)

0 (0%) 40 (100%)

0 (0%) 16 (100%)

0.443

1 (3.8%) 25 (96.2%)

1 (2.5%) 39 (97.5%)

0 (0%) 16 (100%)

0.642

Chi-square test was used *p<0.05; **p<0.01.

Hernias were simply reduced in 98 (51.5%) patients; however, strangulation was detected in 92 (48.5%) patients during the surgery. Whereas intestinal blood circulation recovered in 55 (29%) patients, 37 (19.5%) patients underwent intestinal resection (33 [17.3%] small intestine and 4 [2.2%] colon) and anastomosis due to necrosis. Omental resection was required in 6 (3.1%) patients. There was a significant difference between genders in terms of hernia types. Inguinal hernia was more common in males, whereas umbilical and femoral hernias were more common in females (p<0.001) (Fig. 1, Table 2). The rate of intestinal resection due to strangulation and necrosis was found significantly higher Cilt - Vol. 18 SayÄą - No. 5

in femoral hernias as compared to the other types of hernia (p<0.005 and p<0.001, respectively) (Table 2). There was no significant difference between the types of hernia in terms of age, morbidity, mortality, or recurrence rates (p>0.05) (Table 2). 90 80

Male

%85

70 Percent (%)

General anesthesia was preferred in 135 (71.0%) and spinal anesthesia in 55 (29.0%) cases. The rate of using general anesthesia was significantly higher in umbilical and incisional hernia surgeries (p<0.001).

%70

%69

60

%57

50 40

%43

30

%31

%30

20 10 0

Female

%15 Inguinal

Femoral

Incisional

Umblical

Fig. 1. Distribution of types of hernia according to genders. 391


Ulus Travma Acil Cerrahi Derg

Table 3. Evaluations according to morbidity

Table 4. Evaluations according to mortality p

Morbidity Positive n (%)

Negative n (%)

Mortality Positive n (%)

p

Negative n (%)

Age <65 4 (14.8%) 105 (64.4%) 0.001** ≥65 23 (85.2%) 58 (35.6%) Gender Male 17 (63%) 106 (65%) 0.835 Female 10 (37%) 57 (35%) Type of hernia Inguinal 14 (51.9%) 92 (56.4%) 0.336 Femoral 2 (7.4%) 14 (8.6%) Incisional 7 (25.9%) 21 (12.9%) Umbilical 4 (14.8%) 36 (22.1%) Concomitant disease Positive 21 (77.7%) 66 (40.4%) 0.001** Negative 6 (22.3%) 97 (59.6%) Intestinal strangulation Positive 22 (81.5%) 70 (42.9%) 0.001** Negative 5 (18.5%) 93 (57.1%) Symptom duration ≤24 hours 6 (22.2%) 114 (69.9%) 0.001** >24 hours 21 (77.8%) 49 (30.1%) ASA I-II 2 (7.4%) 93 (57.1%) 0.001** III-IV 25 (92.6%) 70 (42.9%) Intestinal necrosis Positive 14 (51.9%) 23 (14.1%) 0.001** Negative 13 (48.1%) 140 (85.9%) Anesthesia General 25 (92.6%) 114 (69.9%) 0.017* Spinal 2 (7.4%) 49 (30.1%)

Age <65 0 (0%) 109 (59.2%) 0.005** ≥65 6 (100%) 75 (40.8%) Gender Male 5 (83.3%) 118 (64.1%) 0.427 Female 1 (16.7%) 66 (35.9%) Type of hernia Inguinal 5 (83.3%) 101 (54.9%) 0.443 Femoral 0 (0%) 16 (8.7%) Incisional 1 (16.7%) 27 (14.7%) Umbilical 0 (0%) 40 (21.7%) Intestinal strangulation Positive 4 (66.7%) 88 (47.8%) 0.433 Negative 2 (33.3%) 96 (52.2%) Symptom duration ≤24 hours 1 (16.7%) 119 (64.7%) 0.026* >24 hours 5 (83.3%) 65 (35.3%) Concomitant disease Positive 6 (100%) 81 (44.0%) 0.008** Negative 0 (0%) 103 (56%) ASA score I-II 0 (0%) 95 (51.6%) 0.029* III-IV 6 (100%) 89 (48.4%) Intestinal necrosis Positive 4 (66.7%) 33 (17.9%) 0.014* Negative 2 (33.3%) 151 (82.1%) Anesthesia General 5 (83.3%) 134 (72.8%) 1.000 Spinal 1 (16.7%) 50 (27.2%)

ASA: American Society of Anesthesiologists. Chi-square test was used. *p<0.05; **p<0.01.

ASA: American Society of Anesthesiologists. Chi-square test, Fisher’s exact test were used. *p<0.05; **p<0.01.

Mortality was detected in 6 (3.1%) patients, and the reasons for mortality were congestive cardiac insufficiency in 4, pulmonary embolism in 1, and adult respiratory distress syndrome (respiratory insufficiency) in 1 patient.

Morbidity was detected in 27 (14.2%) patients, and the reasons for morbidity were local wound site complications in 14 (10 wound site infection, 4 seroma), postoperative ileus in 4, testicular edema in 3, atelectasis in 2, pneumonia in 2, and congestive cardiac insuffi-

100

Morbidity (+)

90

Morbidity (–)

80

Percent (%)

70 60 50 40 30 20 10 0

≤24 time

>24 time

Symptom duration

I-II

III-IV ASA

Positive

Negative General

Intestinal necrosis

Spinal

Anesthesia

Positive

Negative

Concomitant disease

Fig. 2. Factors affecting morbidity. 392

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Incarcerated abdominal wall hernia surgery

100 90

Mortality (+)

80

Mortality (–)

Percent (%)

70 60 50 40 30 20 10 0

≤24 time

>24 time

Symptom duration

I-II

III-IV ASA

Positive

Negative General

Intestinal necrosis

Spinal

Anesthesia

Positive

Negative

Concomitant disease

Fig. 3. Factors affecting mortality.

ciency in 2 patients. Concomitant disease was detected in 87 (45.7%) patients. Concomitant diseases included chronic obstructive pulmonary disease (COPD), coronary artery disease, congestive cardiac insufficiency, hypertension, and type 2 diabetes mellitus. The rates of advanced age (≥65 years), strangulation, necrosis, high ASA score (III-IV), symptom duration, and presence of concomitant diseases were found significantly high in the group with morbidity and mortality as compared to the group without morbidity and mortality (Tables 3, 4, Figs. 2, 3). The present study demonstrated that general anesthesia was a risk for morbidity as well (p<0.05). There was a significant difference between hernia types in terms of duration of hospital stay (p<0.01). Duration of hospital stay was found significantly shorter in the inguinal hernia group as compared to the femoral, incisional and umbilical hernia groups (p<0.003, p<0.001 and p<0.004, respectively). No significant difference was found between the femoral, incisional and umbilical hernia groups in terms of duration of hospital stay (Table 5) (p>0.05). Duration of hospital stay was significantly higher in the cases with necrosis as compared to those without necrosis (Table 6) (p<0.001).

mortality following incarcerated AWH surgery remain high. The rates of mortality and morbidity have been reported to be approximately 5% and 20%-30%, respectively.[2,4-6] The results obtained in the present study were consistent with the literature showing a mortality rate of 3.1% and a morbidity rate of 14.2%. Many factors affecting mortality and morbidity have been reported. In the present study, the morbidity rate was the highest in incisional hernia, whereas the mortality rate was the highest in inguinal hernia, and no significant effect of the hernia type was determined (p>0.05). While incarcerated inguinal hernias have been more commonly reported in males, femoral and umbilical hernias are more common in females, and no significant effect of gender on mortality and morbidity has been shown.[2,7] Similarly, in the present study, inguinal hernia was more common in males and femoral and umbilical hernias were more common in females Table 6. Duration of hospital stay according to intestinal necrosis

DISCUSSION Despite the advances in anesthesia, antisepsis, antibiotics, and fluid replacement, the morbidity and

Duration of hospital stay

Intestinal necrosis

Mean±SD

Median

Positive Negative

8.78±6.42 4.63±2.49

4.0 7.0

p 0.001**

Mann-Whitney U test **p<0.01.

Table 5. Evaluation of time of discharge according to the hernia types

Type of hernia

Inguinal Femoral Incisional Umbilical Mean±SD (median) Mean±SD (median) Mean±SD (median) Mean±SD (median)

Time of discharge (days)

4.20±2.23 (4)

7.75±6.84 (5)

6.22±2.61 (6)

6.30±4.51 (5.5)

p 0.001**

Chi square test; **p<0.01.

Cilt - Vol. 18 Sayı - No. 5

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(p<0.001); no significant effect of gender on morbidity (p=0.835) or mortality (p=0.427) was observed. Advanced age (≥65 years) is an effective factor on morbidity and mortality in incarcerated AWH surgeries. [8,9] Alverez et al.[7] reported that postoperative pulmonary and cardiovascular complications were frequently encountered in the elderly, and consequently, the duration of hospital stay was prolonged in such patients. Martínez-Serrano et al.[6] stated that advanced age was an effective factor on morbidity and mortality in incarcerated AWH cases. Likewise, in the present study, it was demonstrated that advanced age had a significant effect on morbidity (p<0.001) and mortality (p<0.005). Of the patients with morbidity, 85.2% were ≥65 years, whereas all patients with mortality were ≥65 years. High ASA score (III-IV) and concomitant diseases are the other factors that affect mortality and morbidity.[7] Gloub et al.[10] reported that high ASA score was one of the most important independent risk factors affecting mortality. A significantly longer hospital stay and a significantly higher morbidity rate have also been reported in elderly patients with ASA class III or IV who underwent emergency hernia repair.[4] The study conducted by Alvarez et al.[7] reported that high ASA score was a factor affecting morbidity and mortality. The present study demonstrated that patients with high ASA score had significant morbidity (p<0.001) and mortality (p=0.029). Late presentation to the hospital is also an important factor for morbidity and mortality since it is likely to form a basis for intestinal necrosis and resection. Ashirov et al.[11] stated that the mortality was high among the femoral hernia cases presenting to the hospital later than 48 hours. Kulah et al.[4] demonstrated that morbidity and mortality rates were increased due to strangulation and necrosis in incarcerated hernia cases presenting to the hospital later as compared to those presenting earlier. Patients presenting to the hospital 24 hours after the development of incarceration accounted for 81.8% of the cases who died. In the present study, 83.3% of the cases who died and 77.8% of the cases with morbidity were the patients who presented to the hospital 24 hours after the development of incarceration. Late presentation to the hospital was attributed to the socioeconomic status of the patient, to presentation to small hospitals that lack a relevant specialist, and to misdiagnosis by the physicians. The present study also demonstrated that late presentation to the hospital had a significant effect on morbidity and mortality (p<0.001 and p=0.026, respectively). General anesthesia has been reported to be one of the factors affecting mortality due to the presence of concomitant disease.[4,7] Derici et al.[5] reported that the type of anesthesia had no effect on mortality, but 394

general anesthesia significantly increased the morbidity as compared to spinal anesthesia. The present study demonstrated that general anesthesia increased the morbidity as compared to spinal anesthesia (p=0.017), but had no significant effect on mortality (p=1.00). Strangulation of a hernia is a surgical emergency and has high mortality. Mortality increases in case there is a need for intestinal resection.[12] Femoral type hernia substantially leads to incarceration and strangulation, and thus requires intestinal resection.[13,14] Among the hernia types, intestinal necrosis is most commonly encountered in femoral hernias. However, no significant effect of the hernia type on mortality and morbidity has been demonstrated.[4,15] Femoral hernia may be misdiagnosed as inguinal hernia, lymphadenopathy, lipoma, or psoas abscess.[16] The rate of incarceration and strangulation has been reported to be 44%-86% in femoral hernias.[8,17] In the present study, the rates of strangulation and necrosis in femoral hernias were found as 87.5% and 62.5%, respectively. In the study conducted by Kurt et al.,[3] intestinal necrosis was most common in femoral hernia cases. In the present study, the rate of necrosis was found significantly higher in femoral hernia cases as compared to the other types of hernia. In the present study, while strangulation was found to have a significant effect on morbidity (p=0.001), it had no significant effect on mortality (p=0.433). However, it was observed that necrosis had a significant effect on both morbidity (p=0.001) and mortality (p=0.014). The duration of hospital stay increases due to necrosis and resection. Kurt et al.[3] reported that the period after the resection due to necrosis was effective on morbidity and prolonged the duration of hospital stay. In the present study, the duration of hospital stay was found to be prolonged in the patients undergoing resection due to necrosis (p=0.001). Necrosis was lowest in inguinal hernia cases, and the time to discharge was shorter as compared to the other hernia types (p<0.001). The gold standard in the surgical treatment of incarcerated AWHs is repair of the hernia with low morbidity and mortality and low recurrence rate in the long-term follow-up. Factors that influence recurrences in hernia surgery include inadequate surgical technique, size of the hernia, obesity, wound site infection, cigarette smoking, diabetes, COPD, advanced age, and the use of steroid.[18-22] Recurrence rate has been reported in the literature as 1-22% for incarcerated inguinal hernias[23,24] and as 1-10% for incarcerated femoral hernias.[25] In the present study, recurrence was determined in totally 8 (4.2%) cases; the recurrence rate was highest in inguinal hernia (n=6, 5.9%) Eylül - September 2012


Incarcerated abdominal wall hernia surgery

as compared to all hernia types. Synthetic grafts have been used in hernia surgery for 30 years. The polypropylene graft is durable and stimulates fibroplasia due to its monofilament structure. It neither triggers infection nor is rejected by the tissues.[26,27] Mesh use has no contraindication in many patients that require intestinal resection. It has been reported that polypropylene meshes can be used safely in inguinal hernia cases that undergo intestinal resection. [28] Polypropylene meshes are resistant against infections due to their macroporous structure and can be used safely in AWH defects. Repair techniques performed using Prolene mesh in anterior AWHs in the hands of experienced surgeons and in accordance with the technique would provide lower morbidity and recurrence rates. In their study, Beltran et al.[29] used mesh in both elective and strangulated hernia repairs and could not find any significant difference in terms of postoperative complications. Bessa et al.[30] stated that there was no difference between elective or emergency mesh use in terms of postoperative complications and that mesh could be used safely. Papaziogas et al.[31] found no difference between inguinal hernia repair with and without mesh in terms of postoperative complications and wound infection. Surgical repair using mesh is the current trend in the treatment of primary or recurrent umbilical hernias in both obese and non-obese adults due to its lower recurrence rate as compared to surgical repair by suturing (1% vs. 11%).[32,33] In conclusion, the present study demonstrated that advanced age (≥65 years), presence of concomitant disease, intestinal strangulation, necrosis and intestinal resection, high ASA score (III-IV), and time from onset of the symptoms were effective on morbidity and mortality. General anesthesia poses a risk for morbidity as well. As AWH is identified, surgery should be performed under elective conditions in order to avoid the risks of emergency surgery.

REFERENCES 1. Fitzgibbons Jr. RJ, Cemaj S, Quinn TH. Abdominal wall hernias. In: Mulholland MW, Doherty GM, Lillemoe KD, Maier RV, Simeone D, Upchurch GR, editors. Greenfields surgery. Scientific principles & practice. 5th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2011. p. 1159-98. 2. Kulah B, Kulacoglu IH, Oruc MT, Duzgun AP, Moran M, Ozmen MM, et al. Presentation and outcome of incarcerated external hernias in adults. Am J Surg 2001;181:101-4. 3. Kurt N, Oncel M, Ozkan Z, Bingul S. Risk and outcome of bowel resection in patients with incarcerated groin hernias: retrospective study. World J Surg 2003;27:741-3. 4. Kulah B, Duzgun AP, Moran M, Kulacoglu IH, Ozmen MM, Coskun F. Emergency hernia repairs in elderly patients. Am J Surg 2001;182:455-9. 5. Derici H, Unalp HR, Bozdag AD, Nazli O, Tansug T, Kamer E. Factors affecting morbidity and mortality in incarcerated abdominal wall hernias. Hernia 2007;11:341-6. Cilt - Vol. 18 Sayı - No. 5

6. Martínez-Serrano MA, Pereira JA, Sancho JJ, López-Cano M, Bombuy E, Hidalgo J; Study Group of Abdominal Hernia Surgery of the Catalan Society of Surgery. Risk of death after emergency repair of abdominal wall hernias. Still waiting for improvement. Langenbecks Arch Surg 2010;395:551-6. 7. Alvarez JA, Baldonedo RF, Bear IG, Solís JA, Alvarez P, Jorge JI. Incarcerated groin hernias in adults: presentation and outcome. Hernia 2004;8:121-6. 8. Oishi SN, Page CP, Schwesinger WH. Complicated presentations of groin hernias. Am J Surg 1991;162:568-71. 9. Heydorn WH, Velanovich V. A five-year U.S. Army experience with 36,250 abdominal hernia repairs. Am Surg 1990;56:596-600. 10. Golub R, Cantu R. Incarcerated anterior abdominal wall hernias in a community hospital. Hernia 1998;2:157-61. 11. Ashirov AA, Malevannyĭ AV. Immediate results of treating strangulated hernias. [Article in Russian] Vestn Khir Im I I Grek 1986;136:37-41. [Abstract] 12. Tiernan JP, Katsarelis H, Garner JP, Skinner PP. Excellent outcomes after emergency groin hernia repair. Hernia 2010;14:485-8. 13. Gallegos NC, Dawson J, Jarvis M, Hobsley M. Risk of strangulation in groin hernias. Br J Surg 1991;78:1171-3. 14. Ihedioha U, Alani A, Modak P, Chong P, O’Dwyer PJ. Hernias are the most common cause of strangulation in patients presenting with small bowel obstruction. Hernia 2006;10:338-40. 15. Nesterenko IuA, Shovskiĭ OL. Outcome of treatment of incarcerated hernia. [Article in Russian] Khirurgiia (Mosk) 1993:26-30. [Abstract] 16. Alimoglu O, Kaya B, Okan I, Dasiran F, Guzey D, Bas G, et al. Femoral hernia: a review of 83 cases. Hernia 2006;10:703. 17. Hachisuka T. Femoral hernia repair. Surg Clin North Am 2003;83:1189-205. 18. Venclauskas L, Maleckas A, Kiudelis M. One-year followup after incisional hernia treatment: results of a prospective randomized study. Hernia 2010;14:575-82. 19. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk EG, Jeekel J. Long-term follow-up of a randomized controlled trial of suture versus mesh repair of incisional hernia. Ann Surg 2004;240:578-85. 20. Luijendijk RW, Hop WC, van den Tol MP, de Lange DC, Braaksma MM, IJzermans JN, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med 2000;343:392-8. 21. Le H, Bender JS. Retrofascial mesh repair of ventral incisional hernias. Am J Surg 2005;189:373-5. 22. Iqbal CW, Pham TH, Joseph A, Mai J, Thompson GB, Sarr MG. Long-term outcome of 254 complex incisional hernia repairs using the modified Rives-Stoppa technique. World J Surg 2007;31:2398-404. 23. Derici H, Unalp HR, Nazli O, Kamer E, Coskun M, Tansug T, et al. Prosthetic repair of incarcerated inguinal hernias: is it a reliable method? Langenbecks Arch Surg 2010;395:575-9. 24. Haapaniemi S, Nilsson E. Recurrence and pain three years after groin hernia repair. Validation of postal questionnaire and selective physical examination as a method of follow-up. Eur J Surg 2002;168:22-8. 25. Naude GP, Ocon S, Bongard F. Femoral hernia: the dire consequences of a missed diagnosis. Am J Emerg Med 1997;15:680-2. 26. Hetzer FH, Hotz T, Steinke W, Schlumpf R, Decurtins M, 395


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Largiader F. Gold standard for inguinal hernia repair: Shouldice or Lichtenstein? Hernia 1999;3:117-20. 27. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. The tension-free hernioplasty. Am J Surg 1989;157:188-93. 28. Wysocki A, Kulawik J, Poźniczek M, Strzałka M. Is the Lichtenstein operation of strangulated groin hernia a safe procedure? World J Surg 2006;30:2065-70. 29. Beltrán MA, Cruces KS. Are the outcomes of emergency Lichtenstein hernioplasty similar to the outcomes of elective Lichtenstein hernioplasty? Int J Surg 2007;5:198-204. 30. Bessa SS, Katri KM, Abdel-Salam WN, Abdel-Baki NA. Early results from the use of the Lichtenstein repair in the man-

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agement of strangulated groin hernia. Hernia 2007;11:23942. 31. Papaziogas B, Lazaridis Ch, Makris J, Koutelidakis J, Patsas A, Grigoriou M, et al. Tension-free repair versus modified Bassini technique (Andrews technique) for strangulated inguinal hernia: a comparative study. Hernia 2005;9:156-9. 32. Arroyo A, García P, Pérez F, Andreu J, Candela F, Calpena R. Randomized clinical trial comparing suture and mesh repair of umbilical hernia in adults. Br J Surg 2001;88:1321-3. 33. Sanjay P, Reid TD, Davies EL, Arumugam PJ, Woodward A. Retrospective comparison of mesh and sutured repair for adult umbilical hernias. Hernia 2005;9:248-51.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):397-404

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.62534

Randomized controlled trial of morphine in elderly patients with acute abdominal pain Akut karın ağrısı olan yaşlı hastalarda morfinin randomize kontrollü bir çalışması Faruk GÜNGÖR,1 Mutlu KARTAL,2 Fırat BEKTAŞ,2 Secgin SÖYÜNCÜ,2 Özlem YİĞİT,2 Ayhan MESCİ3

BACKGROUND

AMAÇ

The objective of this study was to determine the clinically important change in diagnostic accuracy and physical examination in the morphine vs. placebo group.

Bu çalışmanın amacı, morfin ve plasebo gruplarındaki klinik olarak önemli tanısal doğruluk ve fizik muayenedeki değişiklikleri belirlemektir.

METHODS

GEREÇ VE YÖNTEM

Subjects were randomized in a 1:1 ratio to receive a single dose intravenous morphine or placebo in a blinded fashion. Primary outcome measure was to determine if there was a clinically important change in diagnostic accuracy and physical examination in the morphine vs. placebo group.

Hastalar 1:1 oranında kör olarak morfin veya plasebo almak için randomize edildi. Çalışmanın birincil takip verisi, morfin ve plasebo gruplarındaki tanısal doğruluk ve fiziksel incelemede klinik olarak önemli değişiklikler olup olmadığını belirlemektir.

RESULTS

BULGULAR

80 subjects (39 were assigned to morphine and 41 to placebo) were included in the final analysis. Clinically important diagnostic accuracy rate was found to be 80% in the morphine group (31/39) and 78% in the placebo group (32/41), with a difference rate of 2% (95% CI -7% to 13%, p=0.9802. There was a statistically significant change in abdominal rigidity finding (15%) in morphine group in all of the abdominal physical examinations findings; however there was no change in placebo group (0%). The difference between two groups was also statistically significant (95% CI 2.3% to 30.5%, p= 0.031).

Seksen hasta (39 morfin ve 41 plasebo) çalışmaya dahil edildi. Klinik olarak önemli tanısal doğruluk oranı morfin grubunda %80 (31/39), plasebo grubunda %78 (32/41) ve %2’lik bir fark oranı saptandı (güven aralığı [GA] %95, -7% ile 13%, p=0,9802). Morfin grubundaki hastaların tüm fiziksel inceleme bulguları içinde sadece abdominal rijidite bulgusunda (%15) istatistiksel olarak anlamlı değişiklik saptandı, ancak plasebo grubunda herhangi bir değişiklik (%0) yoktu. İki grup arasındaki fark anlamlı idi (GA %95, %2.3 ile %30.5, p=0.031). SONUÇ

CONCLUSION

Administration of opioid analgesia is safe and does not seem to impair clinical diagnostic accuracy in elderly patients with acute undifferentiated abdominal pain. Nevermore, opioids may change the physical examination findings such as abdominal rigidity.

Bu çalışma ile acil serviste opioid analjezi uygulanmasının güvenli olduğu ve akut nonspesifik karın ağrısı olan yaşlı hastalarda klinik olarak önemli tanısal değişikliğe neden olmadığı, fakat hastalarda abdominal rijidite gibi önemli fiziksel inceleme bulgularını değiştirebileceği sonucuna varılmıştır.

Key Words: Analgesia/pain emergency departments.

Anahtar Sözcükler: Analjezi/ağrı kontrolü; klinik değerlendirme; acil servis.

control;

clinical

assessment;

1 Department of Emergency Medicine, Antalya Training and Research Hospital, Antalya; Departments of 2General Surgery, 3Emergency Medicine, Akdeniz University Faculty of Medicine, Antalya, Turkey.

Antalya Eğitim Araştırma Hastanesi Acil Tıp Kliniği, Antalya; Akdeniz Üniversitesi Tıp Fakültesi, 2Acil Tıp Anabilim Dalı, 3Genel Cerrahi Anabilim Dalı, Antalya.

1

Correspondence (İletişim): Fırat Bektaş, M.D. Akdeniz Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Kampüs 07059 Antalya, Turkey. Tel: +090 - 242 - 249 61 78 e-mail (e-posta): fbektas@akdeniz.edu.tr

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Analgesia before surgical consultation has traditionally been an area of controversy and was withheld until a definitive diagnosis was established for fear of masking the symptoms, changing physical findings or ultimately delaying diagnosis and treatment of a surgical condition.[1] Recent studies and systematic reviews have shown that administration of opioid analgesics in adult patients with undifferentiated acute abdominal pain, prior to making a decision and while the diagnostic process was underway, did not increase the risk of inadequate treatment decisions and may have significantly improved patient comfort when compared with a placebo.[2,3] Elderly patients who have undifferentiated acute abdominal pain require careful, timely evaluations and aggressive management because of the high risk and subtle presentations of serious pathologic conditions. [4,5] The evidence supporting the use of analgesia in the elderly with undifferentiated acute abdominal pain is limited and based on clinical experience. The objective of this study was to determine if there is a clinically important change in the diagnostic accuracy and physical examination in the morphine vs. placebo group.

MATERIALS AND METHODS Study Design In this single-center, prospective, randomized, double-blind, placebo-controlled clinical trial, elderly patients with undifferentiated acute abdominal pain were divided into two groups, receiving either intravenous morphine or placebo. Study Setting Study participants were recruited from the emergency department (ED) of a tertiary-care university hospital with an annual census of approximately 80,000 adult visits. Both local and central government ethics committees approved the study protocol and all subjects provided written informed consent. Subjects presenting to the ED between April 1, 2009 and December 31, 2009 on weekdays between 08:00 a.m. and 24:00 p.m., the interval covering the shifts of two attending emergency physicians in the ED, were enrolled into the study. Selection of Participants Elderly (65 years or older) patients with non-traumatic undifferentiated acute abdominal pain of less than 48 hours’ duration were included in the study. Participants were required to have an undifferentiated acute abdominal pain and report either “mild” or greater pain intensity on a four-point verbal rating scale (VRS) or at least 20 mm on a 100 mm vi398

sual analogue scale (VAS). Exclusion criteria included known allergy or contraindication to morphine or any opioid analgesic, hemodynamic instability (systolic blood pressure <100 mmHg), and use of any analgesic within six hours before ED presentation; patients who refused to participate in the study, who were uncooperative with respect to the VAS, who had isolated flank pain or previous study enrollment, and those with known renal, pulmonary, cardiac or hepatic failure were also excluded. Interventions Subjects were randomized in a 1:1 ratio to receive a single dose intravenous morphine (0.1 mg/kg in 100 ml normal saline) or placebo (100 ml normal saline) in a blinded fashion. The randomization schedule, constructed with a random numbers table, was prepared before the beginning of the study by an assistant blinded to the study. Treatment allocation assignments were contained in sealed and labeled envelopes and placed into a box. When the treating physician decided to include a patient into the study, the study nurse drew an envelope from the box randomly and premixed the study drug. A second nurse blinded to the study administered the prepared drug to the patient and recorded the previously labeled drug number on the study form. Methods of Measurements After enrollment, emergency residents gathered basic demographic information of participants using a standardized data collection form. Subjects reported pain intensity on both a 100 mm VAS (bounded by “no pain” and “worst pain”) and a four-point VRS (no, mild, moderate, or severe pain) immediately prior to receiving the study drug, and at 30 minutes after drug administration. Subjects were blinded to their prior reports. Before receiving the study drug, the first attending ED physician evaluated the patient’s history, signs of acute abdomen (abdominal tenderness, abdominal rigidity and rebound tenderness) and determined the three most likely diagnoses for that patient. At that time, study drugs were given as bolus infusion in five minutes. Thirty minutes after drug administration, a second attending ED physician on the same work shift who was blinded to the patient and to the first attending physician’s possible diagnosis, evaluated the patient’s history, signs of acute abdomen (abdominal tenderness, abdominal rigidity and rebound tenderness) and determined the three most likely diagnoses for that patient. The quantification of abdominal signs was stated as present, absent or debatable. The preliminary diagnosis provided by the second physician was made without access to any laboratory or radiographic information in order to minimize diagnostic suspicion bias. After receiving the preliminary diagnosis, if the patients were judged to have inadequate pain relief at 30 Eylül - September 2012


Randomized controlled trial of morphine in elderly patients with acute abdominal pain

Enrollment

Assessed for eligibility (n=385)

Analysis Follow up

Allocation

Randomized (n=81)

Excluded (n=304) • Pain of >48 hours’ duration (n=152) • Patients without working time interval of two attending emergency physicians (n=65) • Use of analgesic within 6 hours (n=35) • Patients refused analgesic treatment (n=28) • Uncooperative with the VAS (n=16) • Refused to participate (n=6) • Hemodynamic instability (n=1) • Known allergy or contraindication to morphine or any opioid analgesic (n=1)

Allocated to Morphine (n=40) Received allocated intervention (n=39) Did not receive allocated intervention (n=1) (Persistent vomiting requiring metoclopramide)

Allocated to placebo (n=41) Received allocated intervention (n=41) Did not receive allocated intervention (n=0)

Lost to follow-up (n=0)

Lost to follow-up (n=0)

Analyzed (n=39) Excluded from analysis (n=0)

Analyzed (n=41) Excluded from analysis (n=0)

Fig. 1. CONSORT diagram, patient flow chart.

minutes, they received rescue drugs such as additional analgesia, proton pump inhibitors, or any other agents deemed appropriate by the first physician treating the patient. The first attending ED physician had no role in determining the diagnostic accuracy. Reports of adverse events were collected spontaneously and categorized as nausea/vomiting, altered mental status, dizziness, hypotension, headache, allergy/pruritus, urinary retention, ventilation failure, and dry mouth. Any additional adverse events were noted as “other” and described on the case report form. A research assistant performed a retrospective medical chart review, recording results of all diagnostic tests, and contacted all subjects by telephone to determine if anyone had a surgical intervention or hospital readmission, had undergone a diagnostic or therapeutic medical procedure, or was consulted to another physician. Final diagnosis was obtained through follow-up at least four weeks after their index ED visit and determined by a convincing radiological or pathological diagnosis, response to medical or surgical intervention, or spontaneous resolution according to the patient’s physician, medical records, or patient self-report. Outcome Measures Our primary outcome measure was to determine if there was a clinically important change in diagnostic accuracy or physical examination in the morphine vs. placebo group. Our secondary outcome measures were to evaluate the analgesic effectiveness and safety of intravenous morphine vs. placebo, the need for resCilt - Vol. 18 Sayı - No. 5

cue drugs at 30 minutes, the presence of at least one adverse event, demographic features, and final diagnosis of the patients. After follow-up information was obtained and patient data were recorded on the Statistical Package for the Social Sciences (SPSS) data chart, two coauthors (a general surgeon and an emergency physician) blinded to the study collaboratively determined the clinically important diagnostic accuracy and change in physical examination. Any disagreement between the preliminary and final diagnosis that might be expected to have an adverse effect on the patient’s general status was defined as a clinically important diagnostic error. If coauthors decided an instance of diagnostic error as clinically important, this was coded “diagnostic discordance” for statistical analysis. When the preliminary diagnosis was determined as accurate or not different from the final diagnosis, this was coded as “diagnostic accuracy” for statistical analysis. Diagnostic accuracy was determined between the second attending physician’s preliminary diagnosis and final diagnosis of the patients. Data Analysis All statistical analyses were performed using SPSS version 15.0 for Windows and MedCalc for Windows, version 9.3.0.0 (MedCalc Software, Mariakerke, Belgium). Continuous variables were expressed as mean±standard deviation and categorical variables as percentage. Frequent variables were expressed as rates. Comparison of two independent groups was performed by Student t-test while the related com399


Ulus Travma Acil Cerrahi Derg

parison of two groups was performed by paired t-test for continuous variables. Related comparison of two groups was performed by McNemar test for categorical variables. Kolmogorov Smirnov test was used in order to analyze the distribution of the data as normal or abnormal. To detect a difference of 20 mm with an 80% power and a two-sided level of significance, 37 patients were needed for each group. All the hypotheses were constructed as two-tailed and the critical alpha value was accepted as 0.05.

RESULTS Three hundred and eighty-eight consecutive patients were assessed for eligibility, and 304 patients met one of the exclusion criteria and one patient was not included into the analysis because of protocol violation (Fig. 1). Ultimately, 80 subjects were included into the final analysis: 39 assigned to morphine and 41 to placebo. Characteristics of Study Subjects The mean age of the study subjects was 73±7 and 46% (n=37) of them were male. The subject groups appeared to be well-matched for baseline characteristics and diagnostic study results. Demographic features of the study groups are shown in Table 1. Main Results The baseline pain intensity was similar in the morphine (75.3±22 mm) and placebo (68.6±28.5 mm) groups. The mean reduction in pain intensity at 30 minutes was statistically significant in both groups:

31.6±29.7 mm in morphine group (p<0.0001; 95% confidence interval [CI] 41.2 to 22.0), and 18.8±28.6 mm in placebo group (p=0.0001; 95%CI -27.8 to -9.7), but the difference between the two groups had a borderline statistical significance (12.8 mm, 95%CI -25.8 to 0.1; p: 0.0529) (Table 2, Fig. 2a, b). The accuracy of the final diagnosis by the second physicians was similar in both groups (80% vs. 78%; 2%, 95%CI: -7% to 13%; p=0.9802, respectively). The abdominal tenderness in the physical examination did not decrease significantly in either group (8%, 95%CI: -3.2% to 7.7% vs. 8%, 95%CI: -5.3 to 12, respectively). Although the reduction in abdominal rigidity was 15% (95%CI: -5.8 to 29.9; p=0.17) in the morphine group, abdominal rigidity increased 5% (95%CI: -13 to 20.4; p=0.77) after the placebo infusion. The difference in reduction rates between the two groups was statistically significant (d: 15%, 95%CI: 2.3% to 30.5%; p= 0.031). Rebound tenderness also decreased in the morphine group (13%, 95%CI -7.62 to 27.3, p=0.266); however, as in abdominal rigidity, the rebound tenderness rate was higher after placebo infusion (10%, 95%CI: -7.5 to 21; p=0.34), and the difference between the two groups was 13% (95%CI: 0.7% to 27.4%; p=0.05) with a borderline statistical significance (Table 3). Forty-three patients (53.7%) were discharged from the ED, and 37 patients (46.3%) were hospitalized. Of

Table 1. Demographic features of the study groups Age (mean±SD) Gender Female Male Hypertension Diabetes mellitus History of an operation History of CAD Vital Signs Systolic blood pressure Diastolic blood pressure Pulse/min Fever ◦C Respiratory rate/min Pulse oximetry Diagnosis Abdominal US Abdominal CT Surgical intervention Plain radiography Follow-up Endoscopy

400

Morphine (n=39)

Placebo (n=41)

p

73.3±7.2

73.1±7.9

0.90

21 (53.8%) 18 (46.2%) 21 (53%) 10 (25.6%) 11 (28.2%) 8 (20.5%)

22 (53.6%) 19 (46.4%) 21 (51.2%) 11 (26.8%) 18 (43.9%) 2 (4.9%)

0.99 0.87 0.95 0.64 0.048

144±24 79±13 83±13 36.6±0.6 18±2 98±2

135±25 74±12 84±16 36.3±0.4 17±2 98±2

0.07 0.07 0.83 0.001 0.52 0.47

19 (48%) 12 (31%) 2 (5%) 3(8%) 10 (26%) 0

17 (41%) 8 (20%) 0 1 (2%) 7 (17%) 1 (2%)

Eylül - September 2012


Randomized controlled trial of morphine in elderly patients with acute abdominal pain

10

10

8

8

6

6

4

4

2

2 0

0

(a)

VAS Baseline

VAS 30th minute

VAS Baseline

(b)

Placebo group

VAS 30th minute

Morphine group

Fig. 2. (a, b) Box and whisker plot of the mean reductions in pain scores at the 30th minute after the treatment. The midlines of the boxes represent the medians and the outline of the boxes represents interquartile ratios. The thin lines inside the boxes are for the 95%CI of the means. The lines above and below the boxes show the minimum and maximum values of each group.

the 37 patients, 15 (20%) were operated and 3 died. The most common diagnosis was biliary tract disease followed by dyspepsia and small bowel obstruction (Table 4). Five (12.8%) patients in the morphine group and 4 (9.7%) in the placebo group were hospitalized within the 15-day follow-up after ED discharge (d: 3%, 95%CI: -12 to 18; p: 0.68). Although none of the study patients complained of

serious side effects, the incidence of side effects was higher in the morphine group, with lack of statistical significance (28% vs. 12%, d: 16%, 95%CI: -4 to 36, respectively; p=0.10) (Table 5). The need for rescue drug did not differ significantly between groups (46% vs. 54%; d: 8%, 95% CI: -15 to 30; p=0.62). The satisfaction was better in the morphine group (70.3±28 mm vs. 44.7±31.3; d: 25.5,

Table 2. The mean reductions in pain intensity in the two groups VAS Scores Initial VAS Score±SD 30th minute VAS Score±SD Mean Reduction in VAS Score±SD 95% CI p value

Morphine

Placebo

75.3±22.1 43.6±31.4 -31.6±29.7 -41.2 to -22.0 <0.0001

68.6±28.5 49.8±28.6 -18.8±28.6 -27.8 to -9.7 <0.0001

SD: Standard deviation; VAS: Visual analogue scale; CI: Confidence interval.

Table 3. Changes in physical examination and diagnostic accuracy after the study drug administration Physical examination findings before and after study drug administration Abdominal tenderness

Morphine group difference within group (95% CI)

Placebo group difference (95% CI)

Difference between two groups (95% CI)

100% vs. 92% d: 8% (-3.2 to 7.7) p=0.25

98% vs. 90% d: 8% (-5.3 to 12) p=0.375

0% (-15 to 14)

Abdominal rigidity

51% vs. 36% d: 15% (-6 to 30) p=0.17

34% vs. 39% d: 5% (-13 to 20.4) p=0.77

15% (2.3 to 30)

Rebound tenderness

38% vs. 25% d: 13% (-7.6 to 27.3) p=0.26

19% vs. 29% d: 10% (-7.5 to 21) p=0.34

13% (0.8 to 28)

Diagnostic accuracy

80%

78%

2% (7% to 13%) p=0.9802

Cilt - Vol. 18 Sayı - No. 5

p=0.68

p=0.03

p=0.05

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Table 4. Final diagnosis, surgical interventions and rehospitalization of the study patients Final diagnosis Biliary tract disease Small bowel obstruction Acid-peptic disease Nonspecific abdominal pain Renal colic Diverticulitis Gastroenteritis Acute coronary syndrome Appendicitis Incarcerated inguinal hernia Splenic infarction Ovarian disease Psoas hematoma Hepatic cyst hydatid Malignancies Pancreatitis Right heart failure (hepatic congestion) Urinary tract infection Surgical intervention Rehospitalization

Morphine

Placebo

9 3 5 4 2 2 3 3 1 2 1 1 0 0 0 0

7 9 7 6 4 1 2 0 1 0 0 0 1 1 1 1

1 0 2 0 8 (20.5%) 7 (17%) 5 (12.8%) 4 (9.7%) d: 3%, 95%CI: -12 to 18 p=0.68

suspect such errors were small and randomization should minimize any impact on study outcomes. Another limitation was the lack of interobserver consistency at the beginning of the study. Although this can be thought to cause differences between the physicians evaluating the study patients, the parameters of the physical examinations detected in the study were routine and classical findings that all physicians learn similarly in their clinical practice; thus, we did not feel that interobserver consistency was necessary for this study. Nevertheless, future researchers can consider this fact before beginning their studies. The time interval between the first and second examinations was also a limitation. We determined an interval of 30 minutes, which may not have been adequate to demonstrate physical examination differences for some patients. New studies with different time intervals or with multiple examination repeats in different time frames can give more information on this point. The final limitation was the lack of a standardized algorithm for evaluating the patients in the study. In fact, there is no universal algorithm for acute abdominal pain as found for acute coronary syndromes. All of the attempts applied to the patients were convenient, scientific and academic interventions necessary for their final diagnosis.

95CI%: 12.3 to 38.8; p=0.0003). Limitations This study had several limitations that should be mentioned. We chose to remove patients from analysis if they required rescue analgesics within the first 30 minutes of the study and if their final diagnosis was unclear. In retrospect, we should have planned an intent-to-treat analysis; however, one patient was excluded from the analysis because of protocol violation. Some adverse effects such as nausea and vomiting may be related to the abdominal pathology rather than the study drug. Although we collected adverse effect data, we did not assess the likelihood that the adverse effect could be attributed to the study drug at the time of data collection. In addition, we did not weigh our subjects and relied on self-report of weight to calculate morphine doses. It is possible that the doses used were based on poor weight estimates; however, we

We designed a placebo-controlled trial to assess the clinically important change in diagnostic accuracy and physical examination in the morphine vs. placebo group. We preferred to use normal saline solution as placebo, as it was colorless and easy to find and prepare. Furthermore, it is essential to use a placebo for designing this kind of study. The use of placebo was not an unethical method because administering placebo could improve subjective and objective outcomes in up to 30-40% of patients with a wide range of clinical conditions beyond the pain.[6] Thus, it is the patient’s perceptions of effective treatment that reduce pain or pain behavior. As a result, pain scores may decrease in the placebo group as well as the intervention group. In our study design, study medication or placebo was administered and then patients were given 30 minutes to achieve pain relief. This methodology was similar

Table 5. Comparison of side effects between the two groups

402

Side effects

Morphine (n, %)

Placebo (n, %)

Difference % (95% CI)

p

Nausea and vomiting Hypotension Headache Fatigue Total

5 (12.8%) 1 (2.6%) 1 (2.6%) 4 (10%) 11 (28)

2 (4.9%) 0 (0%) 1 (2.4%) 2 (5%) 5 (12)

8 (-5 to 21) 2.6 (-2 to 7) 0.1 (-7 to 7) 5 (-6 to 17) 16 (-4 to 36)

0.23 0.30 0.97 0.40 0.10

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Randomized controlled trial of morphine in elderly patients with acute abdominal pain

to that of most previous studies, which have allowed for reassessment of parameters in as early as 15 to 30 minutes. If the patients were judged to have inadequate pain relief at 30 minutes, they then received rescue drugs such as additional analgesia, proton pump inhibitors, or any other agents deemed appropriate by the first physician treating the patient. Intervention time was finished at 30 minutes after the study drug administration. The Institutional Human Studies Committee believed strongly that a study period should not exceed one hour because of the potential dangers of opioid administration and also the need for patients to be able to be “off protocol” relatively quickly so they could receive analgesia as clinically indicated.

DISCUSSION The use of analgesia for acute abdominal pain in emergency departments has been debated for many years. Because of the concerns about masking important physical examination findings or ultimately delaying diagnosis and treatment of a surgical condition, analgesics were withheld in undifferentiated abdominal pain patients. This concept used to be useful and valid in the past when the medical science and diagnostic modalities were limited and mostly invasive. However, in today’s advanced era, with different and noninvasive diagnostic modalities, alleviating the pain with opioid analgesics instead of leaving patients in distress for long periods is more humanitarian and rational. According to our study results, morphine administration to relieve acute abdominal pain in patients over 65 years of age may change physical examination findings such as abdominal rigidity and rebound tenderness, but only the change in abdominal rigidity was statistically significant. Despite the change in the physical examination findings, the final diagnosis of the patients was not changed significantly. In light of the above, morphine administration for pain relief to patients over 65 years of age with acute abdominal pain can be applicable. However, the fact that physical examination findings can change with analgesia should not be forgotten, and further diagnostic tests with high sensitivity and specificity should be ordered for precluding diagnostic errors in patient management. There have been various previous reports in the literature about administrating opioid analgesia for abdominal pain. The outcome measures for these studies vary; however, many of them analyzed diagnostic accuracy, management decisions, pain measurements, adverse events, and changes in physical examination findings. In 1992, Attard et al.[7] conducted a study with papaveretum and measured pain scores, patient comfort and diagnostic accuracy. Since the study subCilt - Vol. 18 Sayı - No. 5

jects were patients with significant abdominal pain who were admitted to the hospital, the results cannot be adapted to ED patients entirely. Nevertheless, as the action of papaveretum is similar with opioids, the study is worthy for showing no significant negative effects of opioids on diagnostic accuracy. In 1999, Vermeulen et al.[8] considered morphine versus placebo in the ED patients who were suspected of acute appendicitis, and the diagnostic accuracy was found to be 89% in the morphine group and 91% in the placebo group. Although the selected patient population of the study impeded the generalization of the results, which the authors of the study determined was a limitation, the strong pain relief and both the patient and physician comfort and satisfaction with morphine streamlined the study results. Similar to these results, Gallagher et al.[3] found high patient comfort in their study, and concluded that morphine administration relieved pain and raised patient comfort without clinically significant diagnostic changes. In correlation with the results stated above, we found high patient satisfaction and pain relief without diagnostic errors in the present study. Despite the belief regarding changes in the physical examination, this variable was reported in only four studies.[9-12] Pace and Burke[9] conducted the first randomized double-blind controlled trial with adequate allocation concealment in ED patients with acute abdominal pain in 1996 and concluded that morphine did not lead to any diagnostic error or physical examination alteration. Contrary to these results, physical examination findings changed in the present study, but did not lead to any diagnostic error. In 1997, Lo Vecchio et al.[10] randomized 48 patients admitted to the ED with acute abdominal pain and measured changes in the physical examination and adverse events. A statistically significant change in the physical examination was noted in both groups receiving analgesics; however, the diagnostic accuracy between the preliminary and final diagnosis was not different, and the authors concluded that no adverse events or delays in diagnosis could be attributed to the administration of analgesics. Although the heterogeneity of the study population and the disparity in groups decreased the power of the statistical analysis, as the authors concluded was a limitation, the concordance in diagnostic accuracy rates between the groups was expressive and similar to those of the present study. Furthermore, the changes in physical examination findings were similar to those determined in the present study. In another study, the changes in physical examination signs were not statistically significant and diagnostic accuracy was unchanged.[11] These results were similar with the present study. Mahadevan et al.[12] randomized 66 ED patients suspected of acute appendicitis with right lower quadrant (RLQ) pain equally to tramadol or 403


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placebo in their double-blind controlled trial in 2000 and measured the presence and absence of seven abdominal signs (tenderness on light and deep palpation, tenderness in RLQ and elsewhere, rebound, cough, and percussion tenderness) before analgesic and 30 minutes after analgesic. The difference between the groups was not statistically significant (RR: 1.27 (95%CI: 0.68 to 2.38). As was to be expected and compatible with the literature mentioned above, abdominal rigidity and rebound tenderness findings differed and decreased in the morphine group in the present study. Furthermore, both abdominal rigidity and rebound tenderness findings increased in the placebo group. Rational explanations for the increase would be the progression of the clinical signs by the time of the second examination or failure to meet the patient’s expectations regarding the alleviation of pain in the waiting period. The statistically significant decrease in abdominal rigidity finding should withhold administering morphine analgesics. On the other hand, the decline in abdominal rigidity in the morphine group could minimize the voluntary rigidity, thus improving the diagnostic process and facilitating the physician’s decisions. The unchanged diagnostic accuracy between the morphine and placebo groups can be considered supporting evidence for the latter opinion. Nevertheless, it is clearly known that whether opioid analgesics are used or not, the diagnostic process in elderly patients with abdominal pain is problematic and complicated and needs the greatest attention. In conclusion, the findings of the present study about diagnostic accuracy are parallel with the literature in adult and pediatric patients. Nonetheless, opioid administration to the elderly with acute abdominal pain has not been studied before. Early administration of opioid analgesia is safe and does not seem to impair clinical diagnostic accuracy in elderly patients with acute undifferentiated abdominal pain. Nevertheless, opioids can change physical examination findings such as abdominal rigidity.

404

Acknowledged This study was supported by Akdeniz University Research and Project Unit.

REFERENCES 1. Owens PL, Barrett ML, Gibson TB, Andrews RM, Weinick RM, Mutter RL. Emergency department care in the United States: a profile of national data sources. Ann Emerg Med 2010 ;56:150-65. 2. Rupp T, Delaney KA. Inadequate analgesia in emergency medicine. Ann Emerg Med 2004;43:494-503. 3. Gallagher EJ, Esses D, Lee C, Lahn M, Bijur PE. Randomized clinical trial of morphine in acute abdominal pain. Ann Emerg Med 2006;48:150-60. 4. Manterola C, Astudillo P, Losada H, Pineda V, Sanhueza A, Vial M. Analgesia in patients with acute abdominal pain. Cochrane Database Syst Rev 2007;3:CD005660. 5. Martinez JP, Mattu A. Abdominal pain in the elderly. Emerg Med Clin North Am 2006;24:371-88, vii. 6. Hróbjartsson A, Gøtzsche PC. Is the placebo powerless? An analysis of clinical trials comparing placebo with no treatment. N Engl J Med 2001;344:1594-602. 7. Attard AR, Corlett MJ, Kidner NJ, Leslie AP, Fraser IA. Safety of early pain relief for acute abdominal pain. BMJ 1992;305:554-6. 8. Vermeulen B, Morabia A, Unger PF, Goehring C, Grangier C, Skljarov I, et al. Acute appendicitis: influence of early pain relief on the accuracy of clinical and US findings in the decision to operate--a randomized trial. Radiology 1999;210:639-43. 9. Pace S, Burke TF. Intravenous morphine for early pain relief in patients with acute abdominal pain. Acad Emerg Med 1996;3:1086-92. 10. LoVecchio F, Oster N, Sturmann K, Nelson LS, Flashner S, Finger R. The use of analgesics in patients with acute abdominal pain. J Emerg Med 1997;15:775-9. 11. Thomas SH, Silen W, Cheema F, Reisner A, Aman S, Goldstein JN, et al. Effects of morphine analgesia on diagnostic accuracy in Emergency Department patients with abdominal pain: a prospective, randomized trial. J Am Coll Surg 2003;196:18-31. 12. Mahadevan M, Graff L. Prospective randomized study of analgesic use for ED patients with right lower quadrant abdominal pain. Am J Emerg Med 2000;18:753-6.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):405-410

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.59376

Treatment of acute and closed Achilles tendon ruptures by minimally invasive tenocutaneous suturing Minimal invaziv tenokutanöz dikişle akut ve kapalı Aşil tendonu yırtığının tedavisi Wenge DING, Weihong YAN, Yaping ZHU, Zhiwei LIU

BACKGROUND

AMAÇ

Achilles tendon rupture is a common injury, and its complications can impair function. Numerous operations have been described for reconstructing the ruptured tendon, but these methods can compromise microcirculation in the tendon and can seriously impair its healing. Suturing with a minimally invasive tenocutaneous technique soon after the rupture and systematic functional exercise can greatly reduce the possibility of complications.

Aşil tendonu yırtığı sık rastlanan bir yaralanmadır, komplikasyonları işlevini bozabilir. Yırtılmış tendonun rekonstrüksiyonu için sayısız operasyon tanımlanmış olmasına rağmen bu yöntemler tendonda mikrosirkülasyonu riske atabildiği gibi tendonun iyileşmesini ciddi derecede bozabilir. Yırtıktan hemen sonra minimal invaziv tenokutanöz teknikle dikiş atma ve sistemik fonksiyonel egzersiz, komplikasyon riskini büyük ölçüde azaltabilir.

METHODS

GEREÇ VE YÖNTEM

Between June 1996 and February 2009, we treated 88 patients (54 males; age range, 21-66 years) with this method.

Haziran 1996 ile Şubat 2009 arasında bu yöntemle 21-66 yaş arası 88 (54 erkek) hasta tedavi edildi.

RESULTS

BULGULAR

After follow-up ranging from 1-7 years, the mean American Orthopedic Foot and Ankle Society ankle-hind foot score was 95 (range, 90-98), and the maximum length of postoperative scarring was 3 cm. One patient re-ruptured his Achilles tendon one year after surgery in an accident, but after 10 months, the repaired tendon was still intact. In another patient, the nervus suralis was damaged during surgery by piercing the tension suture at the near end, causing postoperative numbness and swelling. The tension suture was quickly removed, and the patient recovered well with conservative treatment. No large irregular scars, such as those sustained during immobilization, were present over the Achilles tendon.

Bir ile 7 yıl arası izlemden sonra ortalama (Amerikan Ortopedik Ayak ve Ayak Bileği Derneği (American Orthopedic Foot and Ankle Society) ayak bileği ayak arkası skoru 95 (90-98 arası) ve ameliyat sonrası skarın maksimal uzunluğu 3 cm idi. Bir hasta, cerrahiden 1 yıl sonra bir kazada Aşil tendonunu yeniden yırtmıştı. Ancak 10 ay sonra onarılmış tendon hâlâ sağlamdı. Başka bir hastada uca doğru atılan gerim dikişinin delip geçmesine bağlı olarak nervus suralis zedelendi, ameliyat sonrası his kaybı ve ödeme neden oldu. Bu dikiş hemen çıkartıldı ve hasta konservatif tedaviyle iyileşti. Aşil tendonu üzerinde uzun süre hareketsiz kalanlarda olduğu gibi düzensiz büyük skarlar yoktu.

CONCLUSION

SONUÇ

Minimally invasive percutaneous suturing can restore the original length and continuity of the Achilles tendon, is minimally invasive, and has fewer postoperative complications than other methods.

Minimal invaziv perkütanöz dikiş Aşil tendonunun orijinal uzunluk ve bütünlüğünü sağlayabildiği gibi diğer yöntemlere göre ameliyat sonrası komplikasyonları daha az olan minimal invaziv bir yöntemdir.

Key Words: Ankle; injury; surgery; trauma.

Anahtar Sözcükler: Ayak bileği; yaralanma; cerrahi; travma.

Department of Orthopaedic Surgery, 3rd Affiliated Hospital of Suzhou University, PRC.

Suzhou Üniversitesi 3. Hastanesi, Ortopedi ve Travmatoloji Kliniği, Çin Hak Cumhuriyeti.

Correspondence (İletişim): Weihong Yan, M.D. Ju Qian Street, 185 Changzhou, China. Tel: +0519 - 68871316 e-mail (e-posta): sineboat@126.com

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Despite the fact that acute ruptures of the Achilles tendon account for about 35% of all tendon tears,[1] the optimal treatment is still controversial.[2-5] Proposed techniques can be classified as conservative management, open repair, and percutaneous repair.[6] Some authors strongly recommend conservative management,[5,7] but cast immobilization may lead to elongation of the tendon with reduced strength of the calf muscles, and it carries a high rate of re-ruptures.[8] Open repair of acute and closed ruptures of the Achilles tendon is widely accepted.[9,10] However, surgical complications can influence patients’ functional restoration and quality of life.[11,12] These complications are of particular importance to athletes, who have high requirements for functional restoration.[13] Percutaneous suture of an Achilles tendon rupture is a simple and safe method that has functional results similar to those of open repair and a substantially lower complication rate.[14,15] However, our surgical strategy in treating acute and closed Achilles tendon rupture differs from standard percutaneous approaches in that we use minimally invasive tenocutaneous suturing, “comb” the ruptured Achilles tendon to promote healing, and suture the tendinous sheath completely to preserve the blood supply. We report here our results in treating 88 patients with acute and closed Achilles tendon ruptures with this minimally invasive tenocutaneous suturing. The surgery was followed by regular visits over several years to observe the clinical effects and possible complications of this technique.

MATERIALS AND METHODS We studied all patients with acute and closed Achilles tendon ruptures who underwent minimally invasive tenocutaneous suturing at our institution between June 1996 and February 2009. None of the patients underwent bilateral Achilles tendon repair. Achilles tendon ruptures were diagnosed with magnetic resonance imaging scans (MRI) scans and physical exami(a)

(b)

nation (Fig. 1b, c) by the surgeon. All patients were also followed through clinic visits and telephone calls by our surgeon. Surgical Procedure Surgery was performed within three days of presentation. All patients received continuous epidural anesthesia while in a ventricumbent position with a tourniquet applied above the knee in the exsanguinated foot. In surgery, the surgeon located the rupture gap, placed a 3-cm transverse incision along the rupture site (Fig. 2a), and then cut open the aponeurosis lengthwise. The tendinous sheath was usually complete, and the ruptured end of the Achilles tendon was shaped like a horsetail (Fig. 2b). The hematoma at the ruptured end was removed, and the “horsetails” at the two ruptured ends were combed (Fig. 2c). The skin was pierced with a cutting needle from inside to outside at about 4-5 cm on the side near the ruptured section, and about 2-3 cm at the far side of the ruptured section to avoid the surface projection of the nervus suralis and prevent its damage. Double-stranded #10 thread was passed through the skin and the Achilles tendon. The ankle was put in plantar flexion so that the ends of the tendon overlapped by 2 cm, and the tension suture was knotted outside the skin (Fig. 2c). Before knotting, ankle flexion was confirmed to be the same as that of the contralateral ankle joint so that the tendon could be restored to its original length. The incision was then closed and covered with a rubber urethral catheter to reduce compression on the skin (Fig. 2c). In case of exstrophy of the horsetail thread-like fiber and distention, the incision could be loosely closed with absorbable sutures to bring ends of the tendon into an introversion and to ensure proper continuity in the appearance of the tendon, as well as to reduce scarring. Meanwhile, the aponeurosis and tissues surrounding the tendon were repaired with a 4-0 absorbable suture to maintain circulation (Fig. 2d). A step by step schematic diagram of the surgical technique is shown in Fig. 3. (c)

Fig. 1. The ruptured Achilles tendon of a 19-year-old man. (a) Preoperative scan; (b) Preoperative T1 MRI scan; (c) Preoperative T2 MRI scan. 406

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Treatment of acute and closed Achilles tendon ruptures by minimally invasive tenocutaneous suturing

(a)

(b)

(c)

(d)

Fig. 2. Operative repair of a ruptured Achilles tendon of a 19-year-old man. (a) A 3 cm incision is made over the rupture site; (b) The ruptured end of the Achilles tendon is identified by its horsetail shape; (c) The sutured tendon is covered with a rubber urethral catheter to reduce compression on the skin; (d) The aponeurosis and tissues surrounding the tendon were repaired with a 4-0 absorbable suture.

Postoperative Care After surgery, the knee and ankle were each flexed 30° and immobilized in a plaster cast. A window was left at the Achilles tendon to allow the dressing to be changed. The day after surgery, patients began plantar flexion and dorsal angulation exercises for the metatarsophalangeal and interphalangeal joints and contracting and relaxing exercises for the quadriceps femoris to reduce swelling and prevent the formation of venous emboli. Patients were encouraged to move other parts of their body to prevent atrophy of the quadriceps femoris, strengthen the body’s immunity, and enhance blood circulation at the wound, which helped reduced inflammation and swelling at the surgical site. Patients were also asked to do isometric exercises of the gastrocnemius and musculus soleus. After surgery, patients were allowed to rise from their beds on crutches, but were cautioned not to place weight on the injured leg and to keep the foot in plantar flexion. The cast was changed after 2 weeks, and the degree of plantar flexion was reduced to 15°. After the cast was removed at 4 weeks, patients were inCilt - Vol. 18 Sayı - No. 5

c

g f

a b

d

e

Fig. 3. Step by step schematic diagram of the surgical technique. (a) 3-cm transverse incision along the rupture site; (b) Incision of the aponeurosis lengthwise; (c) The sutured tendon is covered with a rubber urethral catheter. (d) Knot of the tension suture; (e) The aponeurosis and tissues surrounding the tendon were repaired with absorbable suture; (f) Suture in skin; (g) Tension suture was knotted outside the skin.

structed to flex the ankle while in bed. After 8 weeks, patients were allowed to stand with crutches and were encouraged to place some weight on the leg, gradually 407


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(a)

(b)

(c)

Fig. 4. The repaired ruptured Achilles tendon of a 19-year-old man. (a) Postoperative MRI scan. (b) MRI scan of the contralateral, uninjured Achilles tendon. (c) Appearance of the tendon with the heel raised.

increase the degree of flexion and extension, and walk with a thick gauze cushion in the shoe. Full weightbearing was allowed 8 to 10 weeks after surgery. The athletes and opera actors were encouraged to conduct adaptive rehabilitation exercises after the plaster was removed, such as swimming and cycling, and could gradually resume their training after 3-4 months. Steroid and aldosterone drugs were not used during the treatment. Follow-Up Examinations and Endpoints Patients were followed until 2009. Three months after surgery, MRI scans of the ankle were obtained and the healing of the Achilles tendon was visually evaluated by three of the present authors, and the American Orthopedic Foot and Ankle Society’s (AOFAS) ankle-hind foot score was determined for all.[16] In addition, the radiological and visual appearances of the repaired tendon were compared with normal radiological and visual appearance.

RESULTS We identified 88 patients (54 males) ranging in age from 21-66 years (mean, 39.5 years) who were eligible for the study. By profession, 8 (9%) were martial arts actors from the Beijing Opera, 5 (5.68%) were opera teachers, 25 (28.41%) were athletes, 45 (51.14%) were sports fans, and 5 (5.68%) were elderly patients with a slight injury experienced while walking. Most injuries were work-related, but in 2 (2.27%) patients, a direct strike from a heavy object had ruptured the tendon. All patients had recent closed injuries without symptoms of autoimmunization, genetic collagen disorder, contagious diseases, or incomplete neural functions. One patient died and one was lost to follow-up 408

after two months. This patient lost to follow- up was not known. Follow-up for the remaining 86 patients ranged from 1-7 years (mean, 2 years). Postoperative Functional Assessment Of the 88 patients, 78 (88.6%) had an MRI checkup three months after the surgery. In general, check-ups revealed continuity of the Achilles tendon, which was properly repaired and shaped and was close to, or had approached, the imaging result of a normal Achilles tendon (Fig. 4a, b). The raising heel test showed that 83 (94.3%) patients could raise their heels forcefully and that the shape of the Achilles tendon was good (Fig. 4c). Mean AOFAS ankle-hind foot score was 95 (range, 90-98), and the maximum length of postoperative scarring was 3 cm. No large irregular scars, such as those sustained during immobilization, were present over the Achilles tendon. Postoperative Complications One patient re-ruptured the same Achilles tendon one year after surgery in a sports accident. The tendon was repaired with Kessler suturing and purely reverse reinforced suturing of the gastrocnemius. Ten months after repair, the repaired tendon was still intact. In another patient, the nervus suralis was damaged during surgery (possibly by inadvertently piercing the tension suture at the near end), causing postoperative numbness and swelling. The tension suture was quickly removed at the patient’s bedside, external immobilization with the cast was prolonged by two months, and exercise intensity was increased more gradually than in other patients. The symptoms disappeared after four months, and the patient recovered well and has experienced no more ruptures. No other complications, such as infection, skin Eylül - September 2012


Treatment of acute and closed Achilles tendon ruptures by minimally invasive tenocutaneous suturing

necrosis, adhesion between the tendon and skin, formation of a cystic lesion at the tendon, or stiffening of the ankle joint, were found in any patient during surgery or the follow-up visits.

DISCUSSION We treated the ruptured Achilles tendons of 88 patients with our minimally invasive percutaneous suturing. This procedure preserved the original length, continuity, and appearance of the tendon with few postoperative complications. The Achilles tendon is the strongest and largest tendon in the human body. About 15 cm long, it originates from the lower third of the calf and inserts at the midpoint of the tuberosity of the calcaneus. It has a pad of bursa synovialis at the front and back. The tendon has no sheath, only loose reticular tissue that links the tendon with the surrounding aponeurosis. It is vascularized.[17] During surgery, we repaired the aponeurosis to ensure a good blood supply to the tendon. We believe we can achieve better healing by “combing” the horsetail-like ends of the tendon and overlapping them by 2 cm when making the repair. Other percutaneous suturing methods do not straighten the tendon fiber, so we believe these methods are not as strong. Traditional Achilles suturing methods include the steel wire Bunnell method and the mattress suturing method, among many others. These “direct open repairs” of the ruptured tendon can require a large incision, seriously damage tissues around the tendon, impair circulation to the tendon, and predispose the repair to postoperative infection and adhesion. Studies of the blood supply to the Achilles tendon[18,19] revealed that these methods can impair microcirculation inside the tendon and seriously impair healing. In contrast, many surgeons find the modified Kessler suturing and fine-thread intermittent suturing of tendon bundles to be simpler, more efficient, and more practical, and therefore, the preferred method for restoring the Achilles tendon.[20] Furthermore, some research has found that suturing with a minimal percutaneous incision soon after the rupture and systematic functional exercise can greatly reduce the possibility of complications.[21-23] Lansdaal et al. found that minimally invasive Achilles tendon repair in Bunnell’s suture in combination with a functional rehabilitation program is a safe and quick procedure with a low rate of re-rupture and a high level of patient satisfaction. [24,25] Recent studies have found that long-term outcome after minimally invasive Achilles tendon rupture repair is excellent, with a low rate of complications.[26,27] We believe our minimally invasive percutaneous suturing conforms to the anatomical physiological feature of the Achilles tendon and meets the healing Cilt - Vol. 18 Sayı - No. 5

requirements inside the tendon. In particular, the technique has the following advantages: 1) The small incision reduces damage to the tissues surrounding the tendon. We only make a simple repair on the ruptured end to make it neat. This method does not require a regular direct incision that requires strong suturing of the ruptured ends to provide continuous and steady tension. The method provides good blood circulation at the ruptured ends, reduces the possibility of postoperative adhesions, and provides good conditions for tendon repair. 2) We placed tenocutaneous sutures in the healthy part of the tendon, far away from the ruptured end. This method provides steady and continuous tension for the repair of the tendon. This “distant” tension allows the matching of ruptured ends, shares most of the tension at the ruptured end, and avoids the influence of tension on the blood supply to the ruptured ends. 3) The method retains the horsetail shape at the residual end of the ruptured tendon. Overlapping tissues are properly arranged and not directly sutured, which maintains the appearance of the tendon. The overlapping length provides a repair that will not differ greatly from the desired length of the tendon. Moreover, it will not lead to possible shortening of the Achilles tendon caused by “direct open” surgery, and the ankle joint has a better degree of mobility after the surgery. 4) The ruptured ends of the Achilles tendon were repaired using absorbable fine suture to maintain neat matching between the ruptured ends. Hence, knots of regular suturing are not seen at the two ruptured ends of the tendon, and the possibility of infections and postoperative complications is reduced. 5) A gradual functional restoration plan is followed after the surgery. Patients are encouraged to start functional exercise as early as possible to reduce postoperative adhesion as well as to restore function. The goal is restore the level of function that existed before the rupture. In conclusion, minimally invasive tenocutaneous suturing for repair of ruptured Achilles tendons can provide good results with few complications. The method combines features of tension suturing and percutaneous suturing, and it preserves blood circulation to the Achilles tendon through “distant” tension. Through a single neat and accurate incision, the method can restore the original length, continuity, appearance, and function of the tendon. The limitations of our research are that the sample size is small, the outcome assessors are also part of the surgical team, and there were no means of comparing the intervention to other therapies or the outcome status to the preoperative status. However, our research 409


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is hypothesis-generating, and the descriptive statistical findings can be used in the development of future prospective cohort studies and randomized controlled trials.

REFERENCES 1. Józsa L, Kvist M, Bálint BJ, Reffy A, Järvinen M, Lehto M, et al. The role of recreational sport activity in Achilles tendon rupture. A clinical, pathoanatomical, and sociological study of 292 cases. Am J Sports Med 1989;17:338-43. 2. Cetti R, Christensen SE, Ejsted R, Jensen NM, Jorgensen U. Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am J Sports Med 1993;21:791-9. 3. Wills CA, Washburn S, Caiozzo V, Prietto CA. Achilles tendon rupture. A review of the literature comparing surgical versus nonsurgical treatment. Clin Orthop Relat Res 1986;207:156-63. 4. Lo IK, Kirkley A, Nonweiler B, Kumbhare DA. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a quantitative review. Clin J Sport Med 1997;7:207-11. 5. Weber M, Niemann M, Lanz R, Müller T. Nonoperative treatment of acute rupture of the achilles tendon: results of a new protocol and comparison with operative treatment. Am J Sports Med 2003;31:685-91. 6. Maffulli N. Rupture of the Achilles tendon. J Bone Joint Surg Am 1999;81:1019-36. 7. Ingvar J, Tägil M, Eneroth M. Nonoperative treatment of Achilles tendon rupture: 196 consecutive patients with a 7% re-rupture rate. Acta Orthop 2005;76:597-601. 8. Leppilahti J, Puranen J, Orava S. Incidence of Achilles tendon rupture. Acta Orthop Scand 1996;67:277-9. 9. Rothenbühler JM, Korkodelovic B, Regazzoni P. Surgical treatment of Achilles tendon rupture. [Article in German] Z Unfallchir Versicherungsmed 1991;84:25-33. [Abstract] 10. Burchhardt H, Krebs U, Schlemminger R, Stanković P. Rupture of the Achilles tendon. Causes and late results after surgical management. [Article in German] Z Orthop Ihre Grenzgeb 1992;130:109-13. 11. Majewski M, Rickert M, Steinbrück K. Achilles tendon rupture. A prospective study assessing various treatment possibilities. [Article in German] Orthopade 2000;29:670-6. [Abstract] 12. Cretnik A, Kosanovic M, Smrkolj V. Percutaneous versus open repair of the ruptured Achilles tendon: a comparative study. Am J Sports Med 2005;33:1369-79. 13. Yinger K, Mandelbaum BR, Almekinders LC. Achilles rupture in the athlete. Current science and treatment. Clin Podiatr Med Surg 2002;19:231-50, v.

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14. Sirový M, Carda M. Open vs. percutaneous suture repair of the subcutaneous Achilles tendon rupture. [Article in Czech] Rozhl Chir 2007;86:594-9. [Abstract] 15. Doral MN, Bozkurt M, Turhan E, Ayvaz M, Atay OA, Uzümcügil A, et al. Percutaneous suturing of the ruptured Achilles tendon with endoscopic control. Arch Orthop Trauma Surg 2009;129:1093-101. 16. Kitaoka HB, Alexander IJ, Adelaar RS, Nunley JA, Myerson MS, Sanders M. Clinical rating systems for the anklehindfoot, midfoot, hallux, and lesser toes. Foot Ankle Int 1994;15:349-53. 17. Boushel R, Langberg H, Green S, Skovgaard D, Bulow J, Kjaer M. Blood flow and oxygenation in peritendinous tissue and calf muscle during dynamic exercise in humans. J Physiol 2000;524:305-13. 18. Carr AJ, Norris SH. The blood supply of the calcaneal tendon. J Bone Joint Surg [Br] 1989;71:100-1. 19. Ahmed IM, Lagopoulos M, McConnell P, Soames RW, Sefton GK. Blood supply of the Achilles tendon. J Orthop Res 1998;16:591-6. 20. Gabel S, Manoli A 2nd. Neglected rupture of the Achilles tendon. Foot Ankle Int 1994;15:512-7. 21. Gorschewsky O, Vogel U, Schweizer A, van Laar B. Percutaneous tenodesis of the Achilles tendon. A new surgical method for the treatment of acute Achilles tendon rupture through percutaneous tenodesis. Injury 1999;30:315-21. 22. Rebeccato A, Santini S, Salmaso G, Nogarin L. Repair of the achilles tendon rupture: a functional comparison of three surgical techniques. J Foot Ankle Surg 2001;40:188-94. 23. Riedl S, Sandberger L, Nitschmann K, Meeder PJ. Suture of fresh Achilles tendon rupture. Comparison of open with percutaneous suture technique. [Article in German] Chirurg 2002;73:607-14. [Abstract] 24. Lansdaal JR, Goslings JC, Reichart M, Govaert GA, van Scherpenzeel KM, Haverlag R, et al. The results of 163 Achilles tendon ruptures treated by a minimally invasive surgical technique and functional aftertreatment. Injury 2007;38:839-44. 25. Pavic R. The results of 163 Achilles tendon ruptures treated by a minimally invasive surgical technique and functional aftertreatment [Injury 2007;38(7):839-44]. Injury 2008;39:499-500; author reply 500. 26. Metz R, van der Heijden GJ, Verleisdonk EJ, Kolfschoten N, Verhofstad MH, van der Werken C. Effect of complications after minimally invasive surgical repair of acute achilles tendon ruptures: report on 211 cases. Am J Sports Med 2011;39:820-4. 27. Valente M, Crucil M, Alecci V, Frezza G. Minimally invasive repair of acute Achilles tendon ruptures with Achillon device. Musculoskelet Surg 2012;96:35-9.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):411-416

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.76736

Çocuk ve erişkin minör kafa travmalarında kan S100B ile laktatın rolü ve bilgisayarlı beyin tomografisi ile korelasyonu The role of blood S100B and lactate levels in minor head traumas in children and adults and correlation with brain computerized tomography Ahmet Ali SEZER,1 Emine AKINCI,1 Miraç ÖZTÜRK,1 Figen COŞKUN,1 Gülsen YILMAZ,2 Alpaslan KARAKAŞ,2 Talip TOKSÖZ2

AMAÇ

BACKGROUND

Bu çalışmada, kan S100B ve laktat değerlerinin çocuk ve erişkin minör kafa travması sonrasında düzeylerinin belirlenmesi ve bilgisayarlı beyin tomografi (BBT) ile karşılaştırılması amaçlandı.

In this study, we aimed to set levels of blood S100B and lactate and to determine any correlation with brain computerized tomography in minor head traumas in children and adults.

GEREÇ VE YÖNTEM

METHODS

Bu çalışmada, Ankara Eğitim ve Araştırma Hastanesi Acil Servisi’ne başvuran, 100 kafa travması hastası geriye dönük olarak incelendi. BULGULAR

S100B için kesim noktası 0-0,15 ve laktat için 0,9-1,5 alındığında; bireylerin %42’sinde S100B’nin yüksek ve %56’sında laktat’ın yüksek olduğu saptandı. Hastaların %12’si 18 yaş ve altı, %88’i 18 yaş üstündeydi. Yaş grupları arasında S100B ve laktat açısından anlamlı farklılık bulunamadı. BBT ile S100B ve laktat düzeyleri ilişkilendirildiğinde istatistiksel olarak anlamlı ilişki saptanmadı. SONUÇ

This clinical trial is a prospective study including 100 head trauma patients who applied to Ankara Training and Research Hospital emergency service. RESULTS

In this study, cut-off ranges of 0.0-0.15 ug/ml and 0.9-1.7 mmol/L for blood S100B and lactate levels, respectively, were used. S100B level was higher than the cut-off range in 42% of patients and lactate level was higher in 56% of patients. No significant differences were determined between age groups. When the relation between S100B and lactate levels with brain CT was evaluated, no statistically significant relation was determined. CONCLUSION

Buna göre minör kafa travmalarında serum S100B ve laktat yüksekliği belirlenmesi klinik muayene veya BBT kullanımının yerini alamaz ve minör kafa travmalarında S100B ve laktatın prognoz tahminlerinde güvenilir işaretleyiciler olmadığı kanaatindeyiz.

According to our results, in minor head traumas, the determination of elevated serum S100B and lactate levels cannot take the place of clinical examination and the use of cranial CT. Although the patients in our study group had minor head trauma, we do not consider S100B and lactate to be reliable markers for estimating progression.

Anahtar Sözcükler: Laktat; minör kafa travması; s100B.

Key Words: Lactate; minor head trauma; S100B.

Ankara Eğitim ve Araştırma Hastanesi, Acil Tıp Kliniği, 2Biyokimya Bölümü, Ankara.

1

Departments of 1Emergency Medicine, 2Biochemistry, Ankara Training and Research Hospital, Ankara, Turkey.

İletişim (Correspondence): Dr. Emine Akıncı. Şenlik Mah., Baldıran Sok., No: 40/18, 06310, Keçiören, Ankara, Turkey. Tel: +90 - 312 - 355 22 19 e-posta (e-mail): emineakinci@yahoo.com

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Kafa travmalı olgularda travma sonrası meydana gelen intrakraniyal hasarın tespitinde, bazı serum belirteçlerinin etkinliği araştırılmaktadır. S100B, nöron spesifik enolaz (NSE), glial fibriler asidik protein (GFAP), interlökinler gibi bazı işaretleyicilerin öne çıktığı görülmektedir.[1] Bizim acil servisimizde olduğu gibi yoğun hasta başvurusu olan acil servislerde kafa travmalı hasta takipleri, yer, zaman ve maliyet açısından sıkıntı oluşturmakta yeni erken tanı ve takip yöntemlerine ihtiyaç duyulmaktadır. Bu çalışmada, kan S100B ve laktat değerlerinin çocuk ve erişkin minör kafa travması sonrasında düzeylerini ve beyin bilgisayarlı tomografisi (BBT) ile karşılaştırılmasını amaçladık.

GEREÇ VE YÖNTEM Bu çalışma 1 Aralık 2010 ile 30 Nisan 2011 tarihleri arasında Ankara Eğitim ve Araştırma Hastanesi Acil Servis’ine başvuran, çocuk ve yetişkin yaş gruplarındaki hastaların alındığı prospektif bir çalışmadır. Çalışmadan dışlanma ölçütleri: Kafa travması hikâyesinin 24 saatten uzun olması, Serebrovasküler hastalıkla beraber kafa travması, Nöbet hikâyesinin olması, Penetran kafa travmaları.

Tablo 1. Hastalara ilişkin tanımlayıcı değerler (n=100)

Yaş (min-maks) Yaş grubu ≤18 yaş >18 yaş Cinsiyet Kadın Erkek GKS (min-maks) Travma tipi Basit düşme Yüksekten düşme Araç içi trafik kazası Araç dışı trafik kazası Darp Geliş süresi (saat) 0-1 1-3 >3 Beyin bilgisayarlı tomografisi Normal Kontuzyon Kırık Sonuç Taburcu Yatış

Ort.±SS

Sayı

43,37±20,57

3-87

12 88

15±0,0

39 61 3-15

28 23 19 10 20

77 19 4

96 1 3

99 1

Kan analizi Hastanın acil servise alınmasından ilk 1 saat içerisinde 2,5 cc kan 150 IU lityum heparin içeren enjektöre, 7,5 cc kan normal biyokimya tüpüne alındı. Kan gazı Roche Cobas 221 cihazı ile S100B düzeyleri kemilüminasyon yöntem ile Sangtec S100B kiti kullanılarak LIAISON cihazında çalışıldı. S100B’nin referans aralığı 0-0,15 ug/ml, laktat’tın referans aralığı ise 0,9-1,7 mmol/L olarak kabul edildi. İstatistiksel veriler Elde edilen verilerin istatistiksel değerlendirmesi “SPSS for Windows 15.0” paket programında yapıldı. Değerlendirmelerde kategorik veriler için ki-kare ve Fisher-Exact testi, S100B, laktat düzeylerinin yaş gruplarına göre karşılaştırmasında Student’s t-testi ve Mann-Whitney U-testi, S100B, laktat düzeylerinin diğer kategorik değişkenlerle ilişkilerinde Student’s t-testi, Mann-Whitney U-testi, tekyönlü varyans analizi ve Kruskall-Wallis varyans analizi kullanıldı. Ay-

rıca ölçümle belirtilen değişkenler arasındaki ilişkiler Spearman-Rank korelâsyon analizi ile değerlendirildi. Tanımlayıcı değerler olarak kategorik verilerde frekans ve yüzde değerleri, ölçümle belirtilen değişkenler için aritmetik ortalama±standart sapma değerleri kullanıldı. İstatistiksel anlamlılık sınırı 0.05 olarak alındı.

BULGULAR Araştırmaya alınan bireylerin hepsinde Glasgow koma skalası (GKS) 15 olup, olguların %61’i erkek, %39’u kadındı. Hastaların %12’si ≤18 yaş, %88’i >18 yaş idi. Travma mekanizması açısından bakıldığında, basit düşme ilk sırayı almakta idi (%28), hastaların %77’sinin geliş süresi ise ilk bir saatte olduğu görüldü. Hastaların %96’sının BBT’leri normal sınırlar içerisindeydi, sadece bir hastaya kafa travması nedeniyle yatış yapıldı (Tablo 1).

Tablo 2. S100B ve laktat düzeylerine ilişkin tanımlayıcı değerler S100B Laktat

412

Normal

Yüksek

Ort.±SS

Medyan

Min.-Maks.

58 44

42 56

0,41±1,12 2,12±0,99

0,13 1,80

0,003-6,50 0,90-8,40

Eylül - September 2012


Çocuk ve erişkin minör kafa travmalarında kan S100B ile laktatın rolü ve BBT ile korelasyonu

Tablo 3. Yaş gruplarına göre S100B ve laktat düzeylerine ilişkin tanımlayıcı değerler ve karşılaştırma sonuçları

Yaş grubu

S100B Laktat

≤18 yaş Ort.±SS

>18 yaş Ort.±SS

p

0,63±1,66 (medyan=0,37) 1,79±0,77

0,38±1,04 (medyan=0,13) 2,16±1,01

>0,05 >0,05

Tablo 4. Hastaların geliş süreleri ile S100B ve laktat değerleri arasındaki ilişki Geliş süresi 0-1 1-3 >3

S100B

Laktat

Ort.±SS

p

Ort.±SS

p

0,43±1,13 0,39±1,23 0,13±0,11

<0,05

2,13±0,79 2,09±1,61 1,88±0,75

>0,05

Bireylerin S100B ve laktat değerlerine ilişkin tanımlayıcı değerler Tablo 2’de verilmiştir. S100B için kesim noktası 0-0,15 ve laktat için 0,9-1,5 alındığında; bireylerin %42’sinde S100B’nin yüksek ve %56’sında laktat’ın yüksek olduğu saptandı (Tablo 2). On sekiz yaş ve altı hasta grubunda S100B’nin %33,3’ü ve laktat’ın %41,7’sinde yüksek tespit edilmesine karşın 18 yaş üstü hasta grubunda S100B’nin

%43,2’sinde, laktat’ın %58,0’inde yüksek olduğu saptandı. Yaş grupları arasında S100B ve laktat açısından anlamlı farklılık bulunmadı (Tablo 3). Hastaların geliş süreleri ile S100B ve laktat değerlerine bakıldığında ise geliş süresi >3 saat olanlarda S100B düzeyi <3 saat olanlara göre anlamlı derecede düşük çıktı (p<0,05) (Tablo 4). Eşlik eden yaralanmalara ilişkin dağılımlara bakıldığında %41’inde izole kafa travması, %28’inde vertebra yaralaması, %13’ü toraks yaralanması, %8’inde karın travması, %24’ünde ekstremite yaralanması %37’sinde skalp yaralanması olduğu saptandı. İzole kafa travması olanlarda S100B, olmayanlara göre anlamlı derecede düşük bulundu (p<0.05). Kafa travması ile birlikte başka bir sistem yaralanması olan hastalar değerlendirildiğinde, vertebra travması olanlarda, olmayanlara göre S100B anlamlı derecede yüksekken (p<0.05), göğüs travması ve skalp yaralanması olan hasta grubunda laktat düzeyi anlamlı derecede yüksekti (p<0,01, p<0.05) (Tablo 5). Çoklu travma ve izole kafa travması durumu için BBT ile S100B ve Laktat düzeyleri ilişkilendirildiğinde; istatistiksel olarak anlamlı ilişkiler saptanmamıştır. S100B için izole kafa travması olanlarda özgüllük %74,4, duyarlılık %50 bulunurken, çoklu travma olanlarda ise bu değerler sırasıyla %49,1 ve %100 olarak bulundu. Laktat düzeyi izole kafa travması olanlarda özgüllük %46,2, duyarlılık %50 bulunurken, çoklu travma

Tablo 5. Eşlik eden yaralanmalar ve S100B ve laktat düzeyleri

S100B

Laktat

n

Ort.±SS

p

Ort.±SS

p

41 59

0,13±0,10 0,61±1,43

<0,05

1,99±0,73 2,20±1,13

>0,05

72 28

0,25±0,65 0,83±1,80

<0,05

2,11±1,07 2,13±0,75

>0,05

76 24

0,37±1,07 0,70±1,46

>0,05

2,02±0,70 2,79±2,00

<0,01

92 8

0,43±1,17 0,17±0,20

>0,05

2,12±0,98 2,03±1,08

>0,05

76 24

0,34±0,99 0,64±1,47

>0,05

2,05±0,78 2,33±1,46

>0,05

63 37

0,46±1,24 0,34±0,89

>0,05

1,93±0,65 2,43±1,33

<0,05

İzole kafa travması Evet Hayır Vertebra travması Yok Var Gögüs travması Yok Var Karın travması Yok Var Ekstremite travması Yok Var Skalp yaralanması Yok Var Cilt - Vol. 18 Sayı - No. 5

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Ulus Travma Acil Cerrahi Derg

Tablo 6. Genel, izole ve çoklu olanlarda S100B ve laktat ile BBT sonuçları arasındaki ilişkiler BBT S100B Laktat

İzole kafa travması

Normal

Anormal

p

Normal

Anormal

Normal Yüksek Normal Yüksek

29 (74,4) 10 (25,6) 18 (46,2) 21 (53,8)

1 (50,0) 1 (50,0) 1 (50,0) 1 (50,0)

>0,05 >0,05

28 (49,1) 29 (50,9) 25 (43,9) 32 (56,1)

0 (0) 2 (100) 0 (0) 2 (100)

olanlarda ise bu değerler sırasıyla %43,9 ve %100 olarak bulundu, bu değerler anlamlı değildi (Tablo 6).

TARTIŞMA S100B insan vücudunda metabolize edilmeden böbrekten atılır. S100B’nin yarı ömrü 120 dakikadır. Yaralanma zamanı ile kan örneğinin alınması arasındaki geçen zaman sonuçları etkileyebilmektedir. Literatürde genellikle S100B’nin yarı ömrü 30 dakika olduğu, bazı çalışmalarda 180 dakikaya kadar uzayabileceğini savunulmaktadır.[2] Ancak, çalışmaların çoğunda ilk 3 saatten sonra alınan S100B sonuçlarının güvenilmez olduğu ve çalışma sonuçlarını etkilediği gösterilmiştir.[3] Çalışmamıza alınan hastaların %77’si travma olduktan sonra ilk 1 saatte acil servise başvurmuşlardır. Geliş zamanı ile S100B ilişkisine bakıldığında geliş süresi >3 saat olanlarda S100B düzeyi <3 saat olanlara göre anlamlı derecede düşük çıkmıştır. Bu sonuç literatür ile uyumludur. Hastaların çoğundan ilk saate kan alındığı için elde ettiğimiz sonuçların güvenilir olduğunu düşünmekteyiz. Çalışmamızda yaş grupları arasında S100B açısından anlamlı farklılık yoktu. Özellikle çocuk hastalarda bazal serum S100B seviyesinin belirlenmesini en çok etkileyen parametre hastanın yaşıdır. Geyer ve arkadaşları[4] 1004 çocukta normal serum S100B seviyelerini incelemiş ve referans eğrisini çizmiştir. Gazzolo,[5] bir yaşının altında diğeri ergen dönemde olan iki pik bulmuştur. Tüm bu çalışmalar S100B’nin yaşa bağlı olduğunu kesin olarak göstermiştir ve minör travmatik beyin yaralanmalarında (TBY) S100B ile ilgili çalışmalarda yaşa spesifik referans kullanılması konusundan bahsedilmektedir, ancak bizim çalışmamızda çocuk sayısı az olduğu için yetişkin hastalardan daha farklı referans değerleri almadık.[6] Çocuk TBY’lerinde S100B rolü henüz açıklığa kavuşmamıştır. Yapılan birkaç çalışmada pediatrik TBY’si olan hastalarda bu proteinin erken artışı güvenilir bir nörolojik prognostik veri olarak değerlendirilmemektedir. Çünkü çoğu olgu serilerinde S100B elde edilen en yüksek değerde olsa bile hastaların çoğunda tam bir nörolojik iyileşme görülmüştür.[7] Çalışmamızda çocuk hasta sayımızın az olmasına rağmen sadece 4 çocukta S100B yüksekliği saptadık. Aksini kanıtla414

Çoklu travma

yan çalışmalar olsa da çocuk hastalarda S100B’nin güvenilir bir prognostik endeks olmadığını düşünmekteyiz. Travmalarda S100B seviyesinin değişken olmasının bir diğer nedeni de başka vücut hasarının olmasıdır. S100B sadece beyin değil beyin dışı dokulardan da salınır. S100B astroglia ve nöronlarda yüksek seviyede olsa da, çoklu travma ile birlikte beyin hasarı olanlarda bu biyoişaretleyicinin santral sinir sisteme spesifikliği azdır. Çalışmamızda hastaların %41’i izole kafa travması, %59’u ise çoklu travmalı idi. Hastalarımızda, kafa travmasından sonra en sık etkilenen ikinci bölge %28 oranında vertebralar, üçüncü sıklıkla ekstremitelerdi. Etkilen yaralanma bölgesi ile S100B ilişkisine baktığımızda özellikle vertebra travması olan hastalarda diğer bölge yaralanmalarına göre anlamlı oranda yüksekti. Litertatürde S100B’nin sadece beyin hasarlarında değil, uzun kemik kırığı, yaygın deri hasarı, yağ dokusu hasarı, kas veya eklem hasarı gibi ek sistemik hasarlarında da yükseldiği gösterilmiştir. [6] Bir çalışmada travma hastaları arasında S100B’nin torasik kontüzyon ve kemik kırığından sonra yüksek olduğu gösterilmiştir. Aynı zamanda yanık ve yumuşak doku yaralanması S100B artışına neden olmuştur. Bu bulgular S100B’nin TBY’daki tanısal kesinliğini azaltmaktadır.[8] Literatürdeki S100B ile ilgili bir kısım çalışmalar S100B’nin prognostik indeks olarak kullanılabilirliği ile ilgilidir.[9] Bu konuda ulaşılan sonuçlar çelişkilidir. Piazza ve arkadaşlarının[7] yaptığı çalışmada travma sonrası S100B’nin erken yükselmesini nörolojik surveyi tahmin etmede güvenilir bir marker olmadığı sonucuna varmışlardır. Bunun tersine Wiesmann ve arkadaşlarının[8] çalışmasında ise özellikle ciddi kafa travmalarında serum S100B ve GFAP’ın travma sonrası nörolojik prognoz ile korele olduğunu öne sürmüşlerdir. Klinik bulgular ve BBT ile kombine edildiğinde prognoz üzerine bilgiyi artıracağını savunmaktadırlar. Doku laktatının progresif kötüleşen hücre etkilerine eşlik eden önemli bir özellik olduğunu bulunmuştur. Kafa travmalarında beyin dokusu veya beyin omurlik sıvısındaki laktat miktarının artması hasarın Eylül - September 2012


Çocuk ve erişkin minör kafa travmalarında kan S100B ile laktatın rolü ve BBT ile korelasyonu

şiddeti ile ilişkilidir.[10] Beyin kan akımında erken dönemdeki azalma ve beyin iskemisi beyin dokusundaki laktat seviyesinin artmasına yol açar. Beyin dokusunda ve serebrospinal sıvıdaki kalıcı laktat yüksekliği kötü prognoz belirtisi olabilir.[11] Çoklu travmalı hastalarda arter laktat düzeyi hasarın şiddeti, resüsitasyonun yeterliliği ve prognoz ile ilgili önemli bir parametre olarak yaygın kabul görmektedir.[12] Majör travma geçiren hastaların çoğunda laboratuvar ve radyolojik değerlendirmeler yapılmakla birlikte baz defisiti ve laktat düzeyi beraber kullanılarak ölümcül olabilecek hastaların triyajı yapılabilmektedir. Yoğun travma merkezlerinde baz defisiti ve laktat düzeyi travmalı hastaların yönetiminde sıkça kullanılmaktadır.[13] Lannoo ve arkadaşları[14] l5 şiddetli TBY’si olan hastalardaki artmış serebral laktat düzeyinin mortaliteyi belirlemede önemli olduğunu saptamışlardır. Goodman ve arkadaşları[15] mikro diyalizle belirlenen serebrospinal laktat düzeyi ile serebral hipoksi ve iskemi arasında ilişki olduğunu göstermişlerdir. Bu bulgulara rağmen izole kafa travmalı hastalarda arteryel laktat düzeyinin serebrospinal/santral sinir sistemindeki laktat düzeyini ne kadar yansıttığını araştıran çalışmaların sayısı azdır. Siegel ve arkadaşları 25 kafa travmalı hastada baz defisitinin oksijen ihtiyacını göstermede değişken önemi olan bir işaretleyici olduğunu ve arteriyel baz defisitinin kafa dışı hasarla birlikte olan kafa travmalarında kötü prognozla ilişkili olduğunu göstermişlerdir.[16] Bizim sonuçlarımızda hastaların %55’inde laktat yüksek çıkmış olmasına rağmen, BBT bulguları, klinikle karşılaştırıldığında istatistiksel olarak anlamlı sonuç elde edemedik. Bu durumun hastalarımızın minör kafa travması olmasından kaynaklandığını düşünmekteyiz. Çalışmamızın sonuçları laktat düzeyinin minör kafa travmalarında travmatik beyin hasarını öngörmede yararlı olmadığını göstermiştir. Bizim çalışmamızda BBT ile S100B ve laktat ile ilişkilendirildiğinde istatistiksel olarak anlamlı ilişki saptamadık. S100B için tüm bireyler için özgüllük %59,4, duyarlılık %75,0 bulunurken, laktat için tüm bireyler için özgüllük %44,8, duyarlılık %75,0 bulundu. Bu değerler istatistiksel olarak anlamlı değildi. Bu sonuç Müller ve arkadaşlarının[3] yaptığı çalışma ile benzerdir. Çalışmalarında minör kafa travmaları yönetiminde, GKS 14-15 olan hastalarda üç hastadan biri için BBT kullanımını önlemek için kullanılabilir olduğunu ve sonuçta S100B’nin BBT’nin yerini alamayacağı ancak, BBT için hasta seçiminde BBT’nin gerekli olup olmadığı konusunda destekleyici bilgi sunabileceğini öne sürmüşlerdir. Filippidis’in çocuk hastalar üzerinde yaptığı, orta ciddi kafa travmalı hastalarda S100B’nin kullanımının sınırlı olduğu ancak gereksiz BBT çekimini azaltabileceği sonucuna varmışlardır.[6] Cilt - Vol. 18 Sayı - No. 5

Bizim sonuçlarımıza göre minör kafa travmalarında serum S100B ve laktat yüksekliği belirlenmesi klinik inceleme veya BBT kullanımının yerini alamaz. Ayrıca minör kafa travmalarında S100B ve laktatın prognoz tahminlerinde güvenilir işaretleyiciler olmadığı kanaatindeyiz Yazarların çıkar çatışması yoktur.

KAYNAKLAR 1. Gabbita SP, Scheff SW, Menard RM, Roberts K, Fugaccia I, Zemlan FP. Cleaved-tau: a biomarker of neuronal damage after traumatic brain injury. J Neurotrauma 2005;22:83-94. 2. Bouma GJ, Muizelaar JP, Stringer WA, Choi SC, Fatouros P, Young HF. Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurg 1992;77:360-8. 3. Müller K, Townend W, Biasca N, Undén J, Waterloo K, Romner B, et al. S100B serum level predicts computed tomography findings after minor head injury. J Trauma 2007;62:1452-6. 4. Geyer C, Ulrich A, Gräfe G, Stach B, Till H. Diagnostic value of S100B and neuron-specific enolase in mild pediatric traumatic brain injury. J Neurosurg Pediatr 2009;4:339-44. 5. Gazzolo D, Michetti F, Bruschettini M, Marchese N, Lituania M, Mangraviti S, et al. Pediatric concentrations of S100B protein in blood: age- and sex-related changes. Clin Chem 2003;49:967-70. 6. Filippidis AS, Papadopoulos DC, Kapsalaki EZ, Fountas KN. Role of the S100B serum biomarker in the treatment of children suffering from mild traumatic brain injury. Neurosurg Focus 2010;29:E2. 7. Piazza O, Storti MP, Cotena S, Stoppa F, Perrotta D, Esposito G, et al. S100B is not a reliable prognostic index in paediatric TBI. Pediatr Neurosurg 2007;43:258-64. 8. Wiesmann M, Steinmeier E, Magerkurth O, Linn J, Gottmann D, Missler U. Outcome prediction in traumatic brain injury: comparison of neurological status, CT findings, and blood levels of S100B and GFAP. Acta Neurol Scand 2010;121:178-85. 9. Hergenroeder GW, Redell JB, Moore AN, Dash PK. Biomarkers in the clinical diagnosis and management of traumatic brain injury. Mol Diagn Ther 2008;12:345-58. 10. Oğün CO, Ustün ME, Duman A, Gürbilek M, Genç BO. Correlation between tissue lactate levels and electroencephalogram in evaluating the severity of experimental head trauma. Crit Care Med 2002;30:2123-8. 11. Zehtabchi S, Sinert R, Soghoian S, Liu Y, Carmody K, Shah L, et al. Identifying traumatic brain injury in patients with isolated head trauma: are arterial lactate and base deficit as helpful as in polytrauma? Emerg Med J 2007;24:333-5. 12. de Boussard CN, Lundin A, Karlstedt D, Edman G, Bartfai A, Borg J. S100 and cognitive impairment after mild traumatic brain injury. J Rehabil Med 2005;37:53-7. 13. Nylén K, Ost M, Csajbok LZ, Nilsson I, Hall C, Blennow K, et al. Serum levels of S100B, S100A1B and S100BB are all related to outcome after severe traumatic brain injury. Acta Neurochir (Wien) 2008;150:221-7. 14. Lannoo E, Van Rietvelde F, Colardyn F, Lemmerling M, Vandekerckhove T, Jannes C, et al. Early predictors of mor415


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tality and morbidity after severe closed head injury. J Neurotrauma 2000;17:403-14. 15. Goodman JC, Valadka AB, Gopinath SP, Uzura M, Robertson CS. Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care

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Med 1999;27:1965-73. 16. Siegel JH. The effect of associated injuries, blood loss, and oxygen debt on death and disability in blunt traumatic brain injury: the need for early physiologic predictors of severity. J Neurotrauma 1995;12:579-90.

Eyl端l - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):417-423

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.28158

Erken fasyotominin yılan ısırıkları tedavisindeki etkinliği Effectiveness of early fasciotomy in the management of snakebites Cemal FIRAT, Serkan ERBATUR, Ahmet Hamdi AYTEKİN, Hıdır KILINÇ

AMAÇ

BACKGROUND

Bu çalışmamızda amacımız, yılan sokmalarına bağlı gelişen kompartman sendromlarının tedavisinde, klasik kompartman sendromu kriterlerinden uzaklaşarak yapılan erken fasyotominin hem klinik iyileşmeyi hızlandırdığı hem de ilerleyici doku hasarını azalttığını vurgulamaktır.

The purpose of this study was to emphasize that early fasciotomy performed in the treatment of snakebites in the absence of the classic compartment syndrome criteria accelerates the clinical recovery and reduces the progressive tissue damage.

GEREÇ VE YÖNTEM

METHODS

Yılan ısırması nedeniyle başvuran 14 hasta geriye dönük olarak incelendi. Hastaların 5’i rutin tedavi ile takip edilerek iyileştirildi. Tedaviye yanıt vermeyen 6 hastaya ekstremitede artan ödem, ağrı, peteşi-ekimoz, bül formasyonu, ilerleyici deri nekrozu ve gerilemeyen klinik ve laboratuvar bozukluklar nedeniyle ilk 48 saat içerisinde erken fasyotomi yapıldı. Geç dönemde kompartman tanısı ile kliniğimize sevk edilen 3 hastaya ise başvurduklarında fasyotomi yapıldı. Fasyotomi insizyonları 4 ila 6 gün sonra kapatıldı.

Fourteen patients with snakebite were examined retrospectively. Five of them healed with routine treatments. Six patients who did not respond to the treatment underwent early fasciotomy procedure in 48 hours. All of the patients had edema, pain, ecchymosis, bulla formation, and progressive skin necrosis over the extremity. Fasciotomy was performed in three patients who were referred in the late period with compartment syndrome. Fasciotomy incisions were closed after 4-6 days.

BULGULAR

RESULTS

Erken fasyotomi uygulanan 6 hastada ödemin hızla azaldığı, ekstremite derisindeki lokal nekrozların ilerlemediği gözlendi. Ayrıca bu hastalarda lokal ısı artışı veya ateş gibi toksik belirtiler hızla geriledi. Geç fasyotomi yapılan 3 hastada ise iyileşme hızı erken cerrahi yapılanlarla kıyaslandığında oldukça yavaştı ve kas ve derideki nekrotik ilerleme kısmen geriledi. SONUÇ

Fasyotomi yılan ısırıklarında özel bir yere sahip olup kompartman sendromu olgularında gerekli tüm tedaviler uygulanmalı kliniğin tam olarak oturmasını veya kompartman basıncının eşik değere ulaşmasını beklemeden erken fasyotomi yapılmalıdır. Anahtar Sözcükler: Fasyotomi; kompartman sendromu; yılan ısırıkları.

İnönü Üniversitesi Tıp Fakültesi, Plastik Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, Malatya.

After the early fasciotomy, edema diminished rapidly, the skin became more viable and local necrosis did not progress. Further, the toxic symptoms like local temperature increase and fever also diminished. The healing process in the three patients who underwent late fasciotomy was much slower compared with the early fasciotomy group. In particular, necrosis on the muscle and skin had deteriorated. CONCLUSION

Fasciotomy has a special place in snakebites. In cases of compartment syndrome, all necessary treatments including early fasciotomy should be performed before the full clinical symptoms develop or the compartment pressure reaches the threshold value. Key Words: Fasciotomy; compartment syndrome; snakebites.

Department of Plastic Reconstructive and Aesthetic Surgery, İnönü University School of Medicine, Malatya, Turkey.

İletişim (Correspondence): Dr. Cemal Fırat. İnönü Üniversitesi Tıp Fakültesi Plastik Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, Malatya, Turkey. Tel: +90 - 422 - 341 06 60 / 5505 e-posta (e-mail): cemal.firat@inonu.edu.tr

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Zehirli hayvan sokmaları dünya genelinde ciddi morbidite ve mortalite nedenlerinden biri olup yılda 4.000.000 insanın yılan sokmasına maruz kaldığı ve bunların 40.000’inin bu nedenle öldüğü tahmin edilmektedir.[1,2] Dünyada mevcut 3000 yılan türünün %10’u zehirlidir.[3] Ülkemizde 40 yılan türü vardır, bunların 10’u zehirli, 2’si yarı zehirli, 28’i zehirsizdir. [1,4] Zehirli 10 yılan türünün 9’u Viperidea ailesinden çıngıraklı engerek yılanı (Vipera ammodytes), diğeri ise Elepidae ailesindendir.[1-5] Viperidae ailesindeki yılan türleri ekstremite ödemi ve kompartman sendromu gibi lokal doku hasarı ve jeneralize ödem, hipotansiyon, gastrointestinal semptomlar, hematolojik, nörolojik ve kardiyak bozukluklar ile renal disfonksiyon gibi sistemik semptomlara neden olabilmektedir.[5] Yılanın zehirsiz olduğu veya yılanın zehrini boşaltamadığı ısırıklara kuru ısırık adı verilmektedir. Yılan zehirlenmelerinde toksisite, yılanın türü, büyüklüğü, zerk ettiği zehir miktarı, ısırık sayısı, ısırılan kişinin yaşı, ısırılan yer ve zehire karşı duyarlılık gibi birçok parametreye bağlıdır.[5,6] Isırılan kişideki sistemik hastalıkların (diabetes mellitus, hipertansiyon, koagülasyon bozuklukları vs. gibi kronik hastalıklar) varlığı ve yaş faktörüne (çocuk ya da yaşlı) bağlı olarak klinik tablo değişkenlik gösterebilir.[3-5] Ülkemizde en sık görülen engerek yılan zehirlenmelerinde ise daha çok lokal ve hematolojik bulgulara rastlanmaktadır.[7] Isırık bölgesinde başlayan ve giderek artan ağrı, ödem, ısı artışı veya ateş, yayılmaya meyilli peteşi ve ekimozlar genel klinik bulgulardır. Yılan ısırıklarında oluşan zehirlenmelerinin tedavisinde acil durumlar dışında genel yaklaşım antiserum tedavisi, tetanoz profilaksisi ve lokal yara bakımıdır. [7,8] Yılan ısırıklarının büyük bir çoğunluğu ekstremitelerde olmakta ve bunların bir kısmında kompartman sendromu gelişmektedir. Literatürde yılan ve böcek

Şekil 1. Isırıktan 72 saat sonra kliniğimize sevk edilmiş bir hastada görünüm. Renkli şekiller derginin online sayısında görülebilir. (www.tjtes.org)

sokmalarına veya travmaya bağlı gelişen kompartman sendromu tedavisi konusunda fikir birliği sağlanamamıştır.[9-16] Cerrahi tedavi için kompartman basıncının eşik değeri konusunda farklı görüşler vardır.[13-16] Bazı çalışmalarda fasyotominin son aşamaya kadar beklenilmesi gerektiği ve fasyotominin oldukça fazla komplikasyonlara yol açabileceği vurgulanmıştır.[9-11] Bu nedenle kompartman sendromunda klinik bulgular tam olarak oturana kadar elevasyon, mannitol tedavisi gibi tıbbi tedaviler uygulanarak beklenebileceği önerilmiştir.[17] Buna karşın diğer bazı çalışmalarda ise ekstremitelerdeki ısırıkların, olası kompartman sendromu açısından sıkı takip edilmesi gerektiği ve klinik olarak şüphelenildiğinde fasyotomi açılması gerektiği görüşü savunulmuştur.[13,18] Kompartman sendromu tanısının gecikmesi iskemik kontraktürlere veya ektremitede çeşitli seviyelerde amputasyonlara neden olmaktadır (Şekil 1).[19]

(a)

(b)

(c)

(d)

(e)

(f)

Şekil 2. (a) Isırıktan 12 saat sonraki görünüm, (b) el bileği dorsomedialinde diş izleri, (c) 36 saat sonra ön kolun görünümü, (d, e) fasyotomiden 12 saat sonraki görünüm. (f) Isırıldıktan 15 gün sonraki görüntü. Renkli şekiller derginin online sayısında görülebilir. (www.tjtes.org)

418

Eylül - September 2012


Erken fasyotominin yılan ısırıkları tedavisindeki etkinliği

Bu çalışmada, yılan sokmalarına bağlı gelişen kompartman sendromlarının tedavisinde, klasik kompartman sendromu kriterlerinden uzaklaşarak daha çok proflaktik amaçlı planlanan fasyotominin hem klinik iyileşmeyi hızlandırdığı hem de ilerleyici doku hasarını azalttığı yönündeki klinik tecrübelerimizi sunmayı amaçladık.

GEREÇ VE YÖNTEM Bu çalışmada Ağustos 2009 ile Ekim 2011 tarihleri arasında kliniğimize yılan ısırması nedeniyle başvuran 14 hasta geriye dönük olarak incelendi. Hastalardan 5’i rutin tedavi ile izlendi, 9’una cerrahi girişim yapıldı. İki çocuk hasta öldü. Hastaların demografik özellikleri, ısırığın yeri, ısırıldıktan sonra geçen süre, kliniğimizdeki izlem süresi, Tablo 1’de özetlenmiştir. Hastaların çoğuna ilk başvurdukları merkezlerin acil servislerinde ilk müdahaleleri yapılmış, tetanoz proflaksisi, antiserum tedavisi uygulanmıştı. Yılan ısırması sonrasında hastalar kliniğimize yatırılarak tedavi altına alındılar. Hastaların kliniğine göre antiserum tedavisine devam edildi. Hastaların kan sayımları, kanama ve pıhtılaşma zamanları, biyokimya değerleri, idrar analizleri ve kardiyak parametreleri 8 saat aralıklarla monitörize edildi. Kompartman sendromu

proflaksisi amacıyla mannitol tedavisi uygulandı. Ekstremitede artan ödem, ağrı, peteşi-ekimoz, bül formasyonu, ilerleyici deri nekrozu ve gerilemeyen klinik ve laboratuvar bozukluklar nedeniyle fasyotomi yapıldı. Bu hastalarda kompartman sendromu için gerekli bulguların tam olarak gelişmesi beklenilmeden 6 hastaya ilk 48 saat içerisinde erken fasyotomi açıldı. Üç hasta ise başvurduğunda kompartman sendromunun tüm kriterlerini taşıyordu. Hiçbir hastaya kompartman basınç ölçümü testi yapılmadı. Fasyotomi açılan hastalar 4 ila 6 gün bekletilerek pansumanla takip edildi ve sonrasında fasyotomi kesisi kapatıldı. Dört hastada greftle onarım gerekirken erken cerrahi yapılan 5 hastada primer onarım yapıldı.

BULGULAR Kliniğimize başvuran 14 hastanın 5’ine sadece tıbbi tedavi uygulandı ve herhangi bir cerrahi işleme gerek duyulmadı. Bu hastaların bir kısmında kuru ısırık olabileceği veya tedavinin etkin sonuç vermiş olabileceği düşünüldü. Erken fasyotomi uygulanan 6 hastada ödemin hızla azaldığı, kas dokusundaki siyanotik kanama odaklarının veya iskemik sahaların gerilediği, ekstremite derisinin daha canlı hale geldiği ve derideki lokal nekrozların ilerlemediği gözlendi. Ayrıca bu

Tablo 1. Hastaların demografik ve klinik özellikleri No

Yaş / Cinsiyet

1 2 3 4 5 6 7 8 9 10 11 12 13 14

3/E 73/K 48/E 24/E 8/K 14/K 55/E 12/K 60/E 26/K 1/E 35/E 23/E 48/K

Isırığın yeri

Isırıktan sonra geçen süre

Tedavi yöntemi

İzlem süresi

Sol bacak laterali Sağ el bileği dorsali Sağ el 2. parmak Sağ bacak laterali Sağ kol mediali Sol bacak postero lateral tibial bölge Sağ el bileği radial taraf Sağ ayak bileği Sağ el 1. parmak pulpası Sağ el 2. parmak Sağ el dorsumu Sağ ayak bileği Sol el 1. parmak Sağ önkol volar yüz

5 gün 12 saat 30 saat 24 saat 4 gün 6 gün 6 saat 36 saat 6 saat 4 saat 24 saat 2 saat 6 saat 6 gün

Rutin tedavi 36. satte fasyotomi+ rutin tedavi 36. satte fasyotomi+ rutin tedavi 48. satte fasyotomi+ rutin tedavi Fasyotomi+rutin tedavi 6. gün fasyotomi+ rutin tedavi Rutin tedavi 3. gün fasyotomi+ rutin tedavi 24. satte fasyotomi+ rutin tedavi Rutin tedavi 48. satte fasyotomi+ rutin tedavi Rutin tedavi Rutin tedavi 6. gün fasyotomi+ rutin tedavi

5. gün ölüm 3 ay 1 ay 3 ay 2 ay 1.5 ay 1 ay 2 2 ay 4. gün ölüm

Cilt - Vol. 18 Sayı - No. 5

1 ay 3 hafta 3 ay

Komplikasyon

Fasyotomi hattında skar Fasyotomi hattında skar 2. parmak pıp eklemden amputasyon Fasyotomi hattında skar Greftlenen alanlarda skar pigmentasyon değişiklikleri Fasyotomi hattında skar Fasyotomi hattında skar Fasyotomi hattında skar Pulpa defekti

Fasyotomi hattında skar

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Ulus Travma Acil Cerrahi Derg

(a)

(b)

Şekil 3. (a) Isırıktan sonra 4. gün görünüm. (b) Dördüncü gün miyonekroz, (c) fasyotomiden 24 saat sonraki görüntü, (d) defektin 15. gün görüntüsü. (c)

(d)

hastalarda lokal ısı artışı veya ateş gibi toksik belirtiler hızla geriledi. Lökositoz, trombositopeni gibi parametreleri bozulmuş olgularda bu değerlerin birkaç gün içerisinde normalleştiği gözlemlendi. Sağ el bileği dorsalinden ısırılan hastada, ısırıktan 36 saat sonra tüm üst ekstremitede aşırı ödem, ağrı, ısı artışı ve koyu renk değişikliği gelişti. El ve önkola yapılan fasyotomi sonrasında hastanın omuzdan itibaren tüm ekstremitedeki şişlik ve ısı artışı geriledi ve laboratuvar değerleri ameliyat sonrası 2. gün normalleşti. Altı gün sonra fasyotomisi kapatıldı (Şekil 2). Sağ kol medialinden ısırılan 8 yaşında kız çocuğuna

(a)

(b)

Renkli şekiller derginin online sayısında görülebilir. (www.tjtes.org)

4. gün tüm üst ekstremite, göğüs duvarı ve boyuna yayılan aşırı ödem, ağrı ve ekimoz nedeniyle önkol, kol ve sternuma fasyotomi açıldı. Fasyotomi sonrası 5 gün içerisinde hastanın ödemi geriledi, renk ve ısı değişikliği giderek soldu (Şekil 3). Hastanın cerrahi öncesi/ sonrası 5. gün laboratuvar değerleri: WBC: 19,1/7, Hb: 5,1/11,4 (transfüzyon), PLT: 114000/438000, CK: 1605/16, LDH: 5062/811, TİT: koyu kırmızı/açık sarı, D-Dimer: 36,8/1,4 idi. Kol medialinde kalan nekrotik saha ve kesi hattı 14 gün sonra greftlenerek onarıldı. Sağ el 1. parmağı ısırılan 60 yaşında erkek hastaya parmakta total siyanoz, antekubital bölgeye kadar

(c)

Şekil 4. (a, b) Isırıktan 6 saat sonra parmağın venöz kanayan, siyanotik görünümü, (c) 24 saat sonra hızlı gelişen ödemin diğer ekstremiteyle karşılaştırmalı görüntüsü. (d, e) Yirmi bir gün sonra fasyotomi hattı ve parmağın görünümü. (d)

420

(e)

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Erken fasyotominin yılan ısırıkları tedavisindeki etkinliği

masif ödem, ağrı, ısı artışı ve eritamatöz renk değişikliği nedeniyle 24 saat sonra parmak, el ve önkola fasyotomi yapıldı. Fasyotomi sonrası ödem, renk ve ısı değişikliği dirsekten itibaren 2 gün içinde geriledi. Parmaktaki nekroz sadece pulpaya lokalize kaldı (Şekil 4). Bu örnek olgular dışında diğer fasyotomi açılan diğer 3 olguda da klinik ve laboratuvar verilerinde aynı sonuçlar gözlemlendi. Kliniğimize başvurduğunda kompartman sendromu tanısı konulup fasyotomi yapılan 3 hastada ise iyileşme hızı erken cerrahi yapılanlarla kıyaslandığında oldukça yavaştı ve kas ve derideki nekrotik ilerleme kısmen geriledi. Ayrıca bu hastalarda aralıklı debridmanlar yapıldı ve tamamı kısmi kalınlıkta deri grefti ile onarıldı. Erken cerrahi uygulanan hastaların 5’inde ödem geçtikten sonra primer onarım ile kesi yeri kapatıldı. Hastaların hiçbirinde uzuv amputasyonu yapılmadı. Bu hastaların hiçbirinde ortalama 3 aylık takiplerinde skar dokusundan kaynaklanan ekstansiyonda hafif çekme dışında kontraktür, kas güçsüzlüğü görülmedi. Greftle onarım yapılan 4 hastada hipertrofik skarlar gözlendi.

TARTIŞMA Yılan ısırmalarında yılanın türünü saptamak her zaman olası değildir. Ölüme kadar varabilen komplikasyonlara neden olabileceğinden, tüm yılan ısırıkları zehirli kabul edilerek izlenmelidir.[20] Kan basıncı kontrol altına alınmalı, kan sayımı, kandaki fibrinojen düzeyi, trombosit sayısı, serum elektrolitleri, kan glukozu, BUN, kreatinin, KCFT, amilaz, CPK, PT, PTT, TİT ve arteriyel kan gazları incelenmelidir. EKG çekilmeli ve incelemeler 8-12 saat arayla tekrarlanmalıdır.[5,7] Zehirli yılan ısırmalarının %30’u tedavi gerektirmez, ısırığın 5-10 cm yukarısında sadece lenfatik akımı engelleyecek kadar bir basınçta ilk 30 dk içerisinde uygulanacak bir turnike zehrin sistemik dolaşıma geçmesini büyük ölçüde azaltır.[21] Yılan zehiri %70 su, %30 proteinli [enzim komponenti ve toksin komponenti] maddeden oluşur.[22] Enzim komponenti hiyaluronidaz ve fosfolipaz A başta olmak üzere oksidaz, esteraz, peptidaz ve proteazdan zengin pıhtılaşmayı bozan bir yapıdadır. Toksin komponenti ise nörotoksinler ve hemotoksinle içerir.[22,23] Nörotoksinler postsinaptik membranda kürar benzeri etki ile diyafram kaslarını etkileyerek ani solunum sıkıntısına yol açabilirken, hematoksinler ise ekstravazasyon, hemoliz, fibrinoliz ya da intravasküler koagülasyona yol açabilir.[22,23] Ülkemizde var olan zehirli yılanların toksini ise daha çok hemolitik özelliktedir.[22] Göğsün üst kısmı ve baş boyun bölgesine yaklaşıldıkça ısırığın tehlikesi artmaktadır. Isırığın damar içine denk gelmesi de zehirin toksisitesini ve morbiditeyi oldukça artırmaktadır. [22] Yılan ısırmaları sonucu görülen lokal bulgular 30 Cilt - Vol. 18 Sayı - No. 5

ila 60 dakika içerisinde ortaya çıkmasına karşın ilk bir hafta içinde kompartman sendromu gelişebilmektedir. [24] Bu yüzden ekstremitelerde olan yılan ısırmalarında oluşabilecek kompartman sendromu açısından sıkı takip gerekmekte ve klinik olarak şüphelenildiğinde fonksiyonel tam iyileşme sağlanabilmesi için fasyotomi yapılmalıdır.[25,26] Zehir, hasarladığı dokudan salınan histamin, bradikinin, serotonin gibi mediyatörlerin artmasına yol açarak etkinliğini artırır.[1,23] Isırıktan sonra başlayan süreç aslında bir kısır döngüdür. Zehir etkinliğini artırdıkça vazodilatasyon amacıyla mediatörler artmakta vazodilatasyon ve vasküler permeabilite arttıkça kompartman içinde ve dışındaki basınç artmaktadır. Sonuçta tek başına dolaşımın yetersizliği nedeniyle nekrotik periyot tetiklenmese bile zehrin lizis ve degredasyon etkisi artmaktadır. Bu nedenle yılan ısırıklarında kompartman basıncı fasyotomi için temel endikasyon olmamalıdır. Diğer travmatik nedenlerle (yanık, kemik fraktürleri vs.) oluşan kompartman sendromlarında basınç ölçümü veya klinik ölçütler ön planda tutulabilir ancak yılan ısırıklarına bağlı kompartman sendromlarında bu ölçütlerin, tüm medikal ve profilaktik tedaviler yapılması şartı ile ikinci planda kalması gerektiğini düşünüyoruz. Fasyotominin kompartman dolaşımını rahatlatma etkisi dışında toksinlerin bu yöntemle aktivasyonlarının azaldığı veya kaybolduğu kanaatindeyiz. Williams ve arkadaşları[13] da ekstremite travmalarının neden olduğu kompartman sendromlarında da erken fasyotominin oldukça etkili ve küratif olduğunu belirtmişlerdir. McQueen ve Court-Brown[27] fasyotomi için eşik basınç değerini 30 mmHg olarak bildirmiştir. Parestezi, solukluk, nabızsızlık, ağrı, pasif hareketle ağrı gibi klinik semptomların oluşmasının beklenilmesi çoğu zaman ya gecikmeye ya da tanıda karışıklığa yol açmaktadır. Anıl ve arkadaşları[17] anti-serum tedavisinin zehrin yıkıcı ekişini ortadan kaldırarak kompartman sendromonu önleyeceğini rapor etmişlerdir. Ayrıca aynı çalışmada mannitol tedavisinin antioksidan etkisi, antiödem etkisi ile nekroz ve apopitozu önlediğini savunmuşlardır. Söz konusu bu tedaviler zaten rutin uygulamalar olup tek başlarına veya kombine olarak etkinlikleri yadsınamaz. Ancak kompartman sendromunu önleme konusunda tamamen küratif olması, kendi olgularımızda ve literatürde yer alan fasyotomi gerekliliği ve sıklığı göz önüne alınacak olursa mümkün gözükmemektedir. Ayrıca antiserum tedavisinin etkinliğinde en önemli belirleyicilerden birinin hastanın zehire olan duyarlılığı olduğu unutulmamalıdır. Yılan ısırmalarının bir kısmında da miyonekroza bağlı bazen lokalize ödem ve ekimoz gelişmekte bazen de nekrotizan fasiit benzeri ilerleyici doku yıkımı gözlenebilmektedir. Bu durumlarda da fasyotomi oldukça küratif olmaktadır. Gold 421


Ulus Travma Acil Cerrahi Derg

ve arkadaşları[11] kompartman basıncı 55 mmHg olan bir olguda mannitol, hiperbarik oksijen ve antiserum kombine tedavisi ile tedavi ettiklerini rapor etmişlerdir. 55 mmHg basınca kadar beklenildiğinde kas dokusu büyük oranda canlılığını kaybedebileceği göz ardı edilmemelidir. Tanen ve arkadaşları[10] yaptıkları domuz çalışmasında tibialis anterior kasları içine direkt yılan zehiri enjekte etmişler ve deneklerin yarısına antiserum diğer yarısına salin vererek fasyotomi yapmışlardır. Fasyotomi yapılanlarda kas nekrozunun daha yüksek olduğunu bulduklarını rapor etmişlerdir. Bu çalışmanın oldukça subjektif oluğu ve direk kas içi enjeksiyon yapılması ve kompartman sendromu kliniğini direkt sağlayamadığı Fulton ve Hoffman[12] tarafından belirtilmiştir. Ayrıca yılan ısırmalarında zehir çoğunlukla kas içine ulaşmaz genellikle subkutan dokuda kalmaktadır. Subkutan dokuda başlayan enflamasyon ile tetiklenen ve kısır döngüyle giderek artan ödem öncelikle ekstrakompartman sahayı etkilemektedir. Lokal doku hasarı zehrin miyotoksik ve sitolitik etkileriyle oluşmaktadır.[23] Ayrıca zehire bağlı oluşan doku nekrozu çinko bağımlı metalloproteinazlar ve miyotoksik fosfolipaz A2 etkisiyle oluşmaktadır.[28] Yılan zehrinin çeşitli nörolojik defisitlere yol açabileceği ya da kompartman sendromu bulgularını taklit edebileceği ve kullanılan çeşitli ağrı kesicilerin kliniği maskeleyeceği de göz ardı edilmemelidir. Yılan sokmalarında sessiz kompartman sendromu gelişebilmektedir. Özellikle çocuklarda klinik bulguların sübjektif olması, çocukların koopere olmamaları ve kompartman basınç ölçümünün kolay yapılamaması gibi nedenlerle tanı gecikmesi olabilir. Bu nedenlerle fasyotomi yılan ısırıklarında farklı endikasyonlara sahiptir. Sonuç olarak, yılan sokmalarından sonra gelişen kompartman sendromu olgularında kliniğin tam olarak oturmasını veya kompartman basıncının eşik değere ulaşmasını beklemeden yapılan erken fasyotomi uygulamaları oldukça etkilidir. Bu olgularda fasyotomi öncesinde gerekli tüm tedaviler uygulanmalı sadece cerrahi daha erken yapılmalıdır. Ayrıca 2. olguda olduğu gibi yılan sokmalarında kompartman sendromu olmadan geç dönemde yapılan fasyotomi nekrotizan fasiit benzeri ilerleyen klinik tabloyu belirgin olarak azaltmakta ve doku yıkımını durdurmaktadır. Yukarıda daha önce belirttiğimiz gibi zehir etkisini enflamatuvar mediatörler üzerinden artırdığı için antihistaminikler, aprotinin (bradikinin salınımını azaltmak için), metiserjid veya ketanserin (serotonin antagonistleri), antioksidanlar (allopurinol, deferoksamin, viamin C-E…), montelukast gibi ajanlarla yapılan kombine tedaviler de etkili olabilir. Ayrıca yılan sokması tedavisinde zehrin inaktivasyonu gelişebilecek komplikasyonların önlenmesi ve fasyotomi gerekliliğini azaltmak için daha geniş kap422

samlı deneysel ve klinik çalışmalara ihtiyaç vardır.

KAYNAKLAR 1. Gündüz A, Hasanbaşoğlu A, Topbaş M. Yılan sokması. Akademik Acil Tıp Dergisi 2003;2:43-7. 2. Çetin O. Türkiye sürüngenleri. Available at: http://reptile. fisek.com.tr. 3. Russel F. When a snake strikes. Emerg Med 1990;22:33-43. 4. Büyük Y, Koçak U, Yazıcı YA, Gürpınar SS, Kır Z. Yılan ısırığına bağlı ölüm. Türkiye Klinikleri J Foren Med 2007;4:127-30. 5. Al B, Orak M, Aldemir M, Güloğlu C. Snakebites in adults from the Diyarbakir region in southeast Turkey. Ulus Travma Acil Cerrahi Derg 2010;16:210-4. 6. Russell EF. Snake venom poisoning in the United States. Ann Rev Medb1980;31:247-56. 7. Köse R. The management of snake envenomation: evaluation of twenty-one snake bite cases. Ulus Travma Acil Cerrahi Derg 2007;13:307-12. 8. Davidson TM, Schafer SF. Rattlesnake bites. Guidelines for aggressive treatment. Postgrad Med 1994;96:107-14. 9. Ertem K. Venomous snake bite in Turkey. Eur J Gen Med 2004;1:1-6. 10. Tanen DA, Danish DC, Grice GA, Riffenburgh RH, Clark RF. Fasciotomy worsens the amount of myonecrosis in a porcine model of crotaline envenomation. Ann Emerg Med 2004;44:99-104. 11. Gold BS, Barish RA, Dart RC, Silverman RP, Bochicchio GV. Resolution of compartment syndrome after rattlesnake envenomation utilizing non-invasive measures. J Emerg Med 2003;24:285-8. 12. Kerns W 2nd, Beuhler M, Tomaszewski C. Hydroxocobalamin versus thiosulfate for cyanide poisoning. Ann Emerg Med 2008;51:338-9. 13. Williams AB, Luchette FA, Papaconstantinou HT, Lim E, Hurst JM, Johannigman JA, et al. The effect of early versus late fasciotomy in the management of extremity trauma. Surgery 1997;122:861-6. 14. Cawrse NH, Inglefield CJ, Hayes C, Palmer JH. A snake in the clinical grass: late compartment syndrome in a child bitten by an adder. Br J Plast Surg 2002;55:434-5. 15. Matsen FA 3rd, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartmental syndromes. J Bone Joint Surg Am 1980;62:286-91. 16. Mars M, Hadley GP. Raised compartmental pressure in children: a basis for management. Injury 1998;29:183-5. 17. Anıl BA, Anıl M, Kara OD, Bal A, Ozhan B, Aksu N. Yılan ısırığına bağlı ağır ödem saptanan üç olguda mannitol tedavisi. Türkiye Klinikleri J Med Sci 2011;31:720-3. 18. Grace TG. Closed compartment ischemia and snakebite. West J Med 1988;148:707. 19. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br 2000;82:200-3. 20. Chew KS, Khor HW, Ahmad R, Rahman NH. A five-year retrospective review of snakebite patients admitted to a tertiary university hospital in Malaysia. Int J Emerg Med 2011;4:41. 21. Tanen D, Ruha A, Graeme K, Curry S. Epidemiology and hospital course of rattlesnake envenomations cared for at a tertiary referral center in Central Arizona. Acad Emerg Med 2001;8:177-82. 22. Dökmeci İ. Hayvansal kaynaklı zehirler. In: Dökmeci İ, Dökmeci AH, editör. Toksikoloji zehirlenmelerde tanı ve tedavi. Eylül - September 2012


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4. baskı. İstanbul: Nobel Tıp Kitabevleri; 2005. s. 500-5. 23. Warrell DA. Snake bite. Lancet 2010;375:77-88. 24. Bulut M, Eren S, Ozdemir F, Koksal O, Durmus O, Esen M, et al. Snakebites cases admitted to Uludağ university faculty of medicine emergency department and current management of snake bite. Akademik Acil Tıp Dergisi 2009;8:31-4. 25. Hsu KY, Shih HN, Chen LM, Shih CH. Lower extremity compartmental syndrome following snake-bite envenomation-one case report. Changgeng Yi Xue Za Zhi 1990;13:54-8.

Cilt - Vol. 18 Sayı - No. 5

26. Wagner HE, Barbier P, Frey HP, Janggen FM, Rothen HU. Acute compartment syndrome following snake bite. [Article in German] Chirurg 1986;57:248-52. [Abstract] 27. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br 1996;78:99-104. 28. Gutiérrez JM, Rucavado A, Chaves F, Díaz C, Escalante T. Experimental pathology of local tissue damage induced by Bothrops asper snake venom. Toxicon 2009;54:958-75.

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):424-428

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.98957

Temporal bone fractures: evaluation of 77 patients and a management algorithm Temporal kemik kırıkları: 77 hastanın değerlendirilmesi ve bir yaklaşım algoritması Gökhan YALÇINER,1 Ahmet KUTLUHAN,1 Kazım BOZDEMİR,1 Hüseyin ÇETİN,2 Behçet TARLAK,1 Akif Sinan BİLGEN1

BACKGROUND

AMAÇ

We aimed to evaluate the etiologies, otolaryngological features, radiological findings, management strategies, and outcomes of temporal bone fractures.

Temporal kemik kırığı olan hastalarda etyoloji, otolaringolojik semptom ve bulguların radyolojik değerlendirmeleri, tedavi yaklaşımları ve sonuçlar değerlendirildi.

METHODS

GEREÇ VE YÖNTEM

Seventy-seven temporal bone fracture cases were retrospectively evaluated for age and gender distribution, side of the fracture, etiology of injuries, the presence of blood otorrhea, tympanic membrane perforation, cerebrospinal fluid otorrhea, hearing loss, hemotympanum, and facial or other cranial nerve palsies, and computerized tomography reports.

Yetmiş yedi temporal kemik kırığı olgusu, yaş, cinsiyet, kırığın yeri, kırığın etyolojisi ve kanlı otore, timpanik membran perforasyonu, serebrospinal otore, işitme kaybı, hemotimpanum, fasiyal ve diğer kraniyal sinir paralizilerinin varlığı ve bilgisayarlı tomografi sonuçları yönünden geriye dönük olarak değerlendirildi.

RESULTS

BULGULAR

Nearly 55% of the cases were caused by traffic accidents and were predominantly male (76.6%). Otolaryngological presentations in order to frequency were early conductive hearing loss (65.8%), blood otorrhea (61.2%), hemotympanum (58.5%), tympanic membrane perforation (25.6%), facial nerve paralysis (12.3%), cerebrospinal fluid otorrhea (8.5%), and sensorineural hearing loss (5.4%). Most of the fractures were petrous (65.8%) and longitudinal type (51.2%).

Olgularda kırıkların %55’i trafik kazası sonucu meydana gelmişti ve çoğunluğu erkekti (%76,6). Otolaringolojik bulgular sıklık sırası ile erken dönem iletim tipi işitme kaybı (%65,8), kanlı otore (%61,2), hemotimpanum (%58,5), timpanik membran perforasyonu (%25,6), fasiyal sinir paralizisi (%12,3), serebrospinal otore (%8,5) ve sensörinöral işitme kaybı (%5,4) idi. Kırıkların çoğu petroz (%65,8) ve uzunlamasına tip (%51,2) idi.

CONCLUSION

SONUÇ

In this research, otolaryngological findings in order of frequency and treatment approaches were compared with literature findings and discussed in 77 temporal bone fracture cases. We formed a management algorithm for the systematic evaluation and treatment of temporal fractures.

Bu araştırmada 77 temporal kemik kırığı hastasında sıklık sırası ile otolaringolojik bulguları ve tedavi yaklaşımımızı literatür bulguları ile karşılaştırıp tartıştık. Temporal kırıklarda sistematik bir değerlendirme ve tedavi için bir algoritma oluşturduk.

Key Words: Head trauma; maxillofacial injuries; temporal bone.

Anahtar Sözcükler: Kafa travması; maksillofasiyal yaralanma; temporal kemik.

Departments of 1Otolaryngology, 2Radiology, Ankara Atatürk Training and Research Hospital, Ankara, Turkey.

Ankara Atatürk Eğitim ve Araştırma Hastanesi 11. KBB Kliniği, Radyoloji Kliniği, Ankara.

Correspondence (İletişim): Gökhan Yalçıner, M.D. Ankara Atatürk Eğitim ve Araştırma Hastanesi, 1. KBB Kliniği, Bilkent Yolu Lodumlu Mevkii No: 2, 06800 Ankara, Turkey. Tel: +090 - 312 - 291 25 25 / 4338 e-mail (e-posta): gkhnyalciner@yahoo.com

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Temporal bone fractures

Nowadays, head trauma is a common injury to which all of us are susceptible because of high speed travel.[1] Skull fractures affect 23%-66% of patients with head trauma and approximately 4%-30% of head injuries involve a fracture of the cranial base, including 18%-75% of temporal bone involvement.[2,3] After a severe head injury, the maintenance of life is the most important concern. After providing stable vital functions like breathing, circulation and neurosurgical evaluation and evaluation of the chest and abdomen, it is appropriate for an otolaryngologist to evaluate the patient. The importance of temporal bone fractures according to the otolaryngologist is the facial nerve and the structures related to hearing and balance located therein and prevention of functional losses. The most common physical examination findings of temporal bone fractures are blood otorrhea, tympanic membrane perforation, hearing loss, hemotympanum, cerebrospinal fluid (CSF) otorrhea, and facial and other cranial nerve palsies. In this research, we retrospectively reviewed the causes, gender distribution, otolaryngological features, radiological findings, and outcomes of 77 temporal bone fracture cases between March 2007 and April 2011.

MATERIALS AND METHODS Seventy-seven patients who were evaluated and treated for temporal bone fracture by our clinic between March 2007 and April 2011 and whose required data were obtained from their files were included in this retrospective research. Age, gender distribution, side of fracture (right, left, bilateral), etiology of injuries, presence of blood otorrhea, CSF otorrhea, tympanic membrane perforation, hearing loss (conductive, sensorineural or mixed), hemotympanum, and facial and other cranial nerve palsies, computerized tomography (CT) reports, and follow-up results were evaluated. The collected data were then analyzed and compared with the literature series. RESULTS Ages of the patients ranged from 8-76 years. Age, gender distribution, side of the fracture, and etiology of the injuries are seen in Table 1. In addition to the otolaryngologic examination, all patients were evaluated with axial and coronal CT. In CT, the fractures were evaluated according to two different classification systems as petrous-non-petrous and transverselongitudinal-oblique-mixed. The presence of blood otorrhea, tympanic membrane perforation, hearing loss (conductive-sensorineural-mixed), hemotympanum, CSF otorrhea, and facial and other cranial nerve palsies was noted according to the above classification systems. Cilt - Vol. 18 SayÄą - No. 5

Table 1. Distribution of cases according to age, gender, fracture side and mechanism of injury Total

n

%

Age

3 10 28 12 10 8 5 1 59 18 38 34 5 42 19 12 3 1

3.89 12.98 36.36 15.58 12.98 10.38 6.49 1.29 76.62 23.37 49.35 44.15 6.49 54.54 24.67 15.58 3.89 1.29

8-10 11-20 21-30 31-40 41-50 51-60 61-70 71+ Gender Male Female Side Right Left Bilateral Mechanism Traffic accidents of injury Falls Industrial accidents Assault Gunshot wound

The facial and other cranial nerve palsies that were found in the first examination were counted as immediate and those found later (after the first few hours) were evaluated as late. The patients who were unconscious and were not appropriate for evaluation of hearing loss and facial function were ignored during the calculation of the percentages. Therefore, when calculating hearing loss and facial and other nerve functions, the total number of fractures was accepted as 73, and the other ratios were calculated on the basis of 77 patients with 82 temporal fractures (5 patients had bilateral fractures). Results are seen in Table 2. Fourteen patients died of severe intracranial and other injuries.

DISCUSSION Temporal bone fractures occur from high energy mechanisms, particularly as a result of side impacts, typically but not limited to motor vehicle accidents.[4] In the literature, risk factors for and causes of temporal bone fractures are: younger age, male gender and motor vehicle accidents.[5-8] Similarly, in our series, traffic accidents were the primary mechanism of the injury, with a 54.5% ratio; 76.6% of the cases were male and the mean age was 34.1 years. This result may be related to the fact that young males are greater participants in traffic and industrial business. When otolaryngologists were consulted for the treatment of these patients, their primary concern was the evaluation of the external ear and tympanic membrane, the presence of blood otorrhea and CSF otorrhea, hearing status, facial nerve function, and the presence of hemotympanum. However, not infrequently, the severity of the injury, the patient’s uncon425


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Table 2. Distribution of findings due to two different classification systems Total fracture Blood otorrhea Tympanic membrane perforation Hemotympanum Cerebrospinal fluid otorrhea Conductive hearing loss Sensorineural hearing loss Facial nerve palsy Other cranial nerve (CN III, IV, VI) palsies Meningitis

Total

A (n, %)

B (n, %)

C (n, %)

D (n, %)

E (n, %)

F (n, %)

82 51, 62.1

54, 65.8 43, 52.4

28, 34.2 8, 9.7

42, 51.2 33, 40.2

21, 25.6 11, 13.4

5, 6.1 3, 3.6

14, 17.1 4, 4.8

21, 25.6 48, 58.5

20, 24.3 41, 50

1, 1.2 7, 8.5

12, 14.6 29, 35.3

6, 7.3 12, 14.6

2, 2.4 3, 3.6

1, 1.2 4, 4.8

7, 8.5 50, 64.9 9, 12.3

Immediate Late

6, 7.3 44, 57.1 7, 9.5

1, 1.2 6, 7.8 2, 2.7

4, 4.8 35, 45.4 4, 5.4

1, 1.2 9, 11.6 3, 4.1

– 1, 1.3 –

2, 2.4 5, 6.5 2, 2.7

4, 5.4 3, 4.1 6, 8.2

Immediate Late

4, 5.4 2, 2.7 6, 8.2

– 1, 1.3 –

3, 4.1 – 4, 5.4

1, 1.3 2, 2.7 1, 1.3

– – 1, 1.3

– 1, 1.3 –

2, 2.7 1, 1.3

2, 2.7 1, 1.3

– –

2, 2.7 1, 1.3

– –

– –

– –

A: Petrous; B: Non-Petrous; C: Longitudinal; D: Transverse; E: Oblique; F: Mixed or comminuted.

scious status, and other severe injuries requiring urgent intervention lead to a delay in the otolaryngologic evaluation and management. After a physical examination for the establishment of an accurate fracture diagnosis, axial and coronal temporal CTs have a critical importance.[9,10] We formed a management algorithm for the evaluation of temporal bone fractures. This algorithm format of temporal fracture management may offer a rapid experience opportunity for inexperienced practitioners (Fig. 1). To our best knowledge, no such algorithm has been reported to date. There are several classification systems for the evaluation of temporal fractures with CT. Some of them are longitudinal-transverse-oblique or mixed, petrous–non-petrous, and otic capsule sparing–otic capsule violating.[2,3,6,7] In the different series, statistical correlation between clinical findings and these classifications has been reported.[3,6] In our series, we also evaluated the distribution of clinical findings according to petrous-non-petrous and transverse-longitudinal-oblique-mixed classifications. The distribution of fracture types and clinical findings due to these classifications are seen in Table 2. In our opinion, these classification systems may be important for statistical results, but are not clinically important, as we evaluate the patients according to the existence of the above-mentioned symptoms and findings and not the classification systems. In our research, the most common otolaryngological findings were conductive hearing loss (CHL) in the early period (64.9%), blood otorrhea (62.1%), hemotympanum (58.5%), and tympanic membrane perfora426

tion (25.6%). The hearing loss ratio in the early period is determined by the diapason test results of the first examination. This high ratio may be due to the high rate of hemotympanum and tympanic membrane perforations. After the average 4-6 week follow-up period, in patients with hearing loss, the CHL ratio was 12.3%, which was determined by the audiologic examination. In the literature, the reported incidence rates for CHL were 10%-57%.[3,7] CHL generally resolves over time (usually within 3-4 weeks).[2] Pure hemotympanum generally resolves without sequelae within this time period as well.[2] Small tympanic membrane perforation also heals within 4-6 weeks. If CHL and tympanic membrane perforations persist after 3 months, then tympanoplasty and, if necessary, ossicular chain reconstruction should be performed.[2] The most common ossicular chain disruption is incudostapedial dislocation (11%-14%), followed by dislocation of the incudomallear joint.[3] In our series, 5 patients underwent tympanoplasty, and 2 of them underwent incudostapedial joint repair with bone cement. According to our research, the most common three symptoms (apart from early CHL), blood otorrhea, hemotympanum and tympanic membrane perforation, were seen above the rate of 90% with petrous fractures. Therefore, if a classification system has to be used, petrous-non-petrous classification seems more appropriate for otolaryngological purposes. The sensorineural hearing loss (SNHL) rate was found as 5.4%, and all of these cases were caused by petrous fracture. In the literature, SNHL rates were reported as 0%-14%.[2,7] As is well known, there is no Eylül - September 2012


Temporal bone fractures

Blood otorrhea

Medical history and physical examination -Cause of injury -Consciousness -Other injuries

TEMPORAL TRAUMA

Evaluate/Stabilize -Airway -Circulation -Cervical vertebrae -Major system or life-threatinhg injuries

-Otolaryngological Examination -Temporal bone CT axial-coronal

Laboratory -CBC -Coagulation tests -Radiological evaluation of other injuries -Screening of alcohol and other toxic substances

Insignificant

Aspiration

Massive

Temporary Packing

Tympanic Membran Perforation

Follow-up (3 months)

Haematympanum

Follow-up (3-4 weeks)

CSF otorrhea

-B2 transferrin -Follow-up (2 weeks) -Antibiotics?

Healed Non-healed

Healed Non-healed

Conductive heraing loss

Follow-up (3 months)

Healed

Sensorineural hearing loss

Steroid therapy (?)

Healed

Meningitis

Antibiotics therapy

Other cranial nerve paralysis

Neurosurgical consultation

Persistant

Non-healed

Immediate

Surgical exploration

Late

Corticosteroids

Facial nerve palsy

Tympanoplasty

Surgical repair

Exploration and ossiculer chain reconstruction

Hearing aid or cochlear implant

Healed Non-healed

Electrodiagnostic testing Regeneration signs Non-regeneration signs Follow-up

Exploration

Fig. 1. The algorithm format of temporal bone fracture management.

effective treatment for SNHL, and rehabilitation with hearing aids, and if necessary cochlear implant, is recommended. Although there is not enough data in the literature about the usage of steroids for the treatment of SNHL due to temporal fracture, there is a possibility that they can be applied. We also do not have any experience about such treatment, but we intend to apply it in the future. In our research, there were 9 facial nerve paralysis cases, with 3 of them having early or immediate and 6 having late onset (Fig. 2). All of the 6 paralysis cases with late onset were seen with petrous fractures and 2 of the 3 cases with early or immediate onset paralysis were seen with petrous fractures, while 1 had non-petrous, mixed type fracture. In the literature, facial nerve paralysis rates were reported as 10%-25% for longitudinal fractures and 38%-50% for transverse fractures.[3] For transient and persistent facial paralysis, rates up to 65.5% were also reported.[11] In our series, all of the late onset cases were given corticosteroid therapy and then followed up. All of them almost completely recovered. One of the early onset cases who also had 3rd, 4th and 6th cranial nerve paralysis died. One of them remained unconscious in the neurosurgical intensive care unit for 6 weeks and had septiCilt - Vol. 18 Say覺 - No. 5

cemia. When his general condition improved, he had blindness due to optic atrophy and 3rd and 6th nerve paralysis on the facial paralysis side. His family did not accept surgery for facial nerve exploration.

Fig. 2. CT of a patient with early facial paralysis showing transverse fracture. 427


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During the follow-up of the third patient in the intensive care unit for improvement in general status for the facial exploration operation, on the 20th day, signs of regeneration were detected in the electromyography and the operation decision was abandoned. A generally accepted principle of the treatment of facial paralysis is that the management depends on the timing of paralysis related to the injury.[3] Rapid loss of facial nerve function (immediate or within the first few hours) is likely due to transaction and is traditionally managed with surgical exploration after imaging and electrical studies indicate a need for nerve decompression or repair. On the other hand, a delayed loss is more likely due to edema and is typically treated with high-dose corticosteroids with further intervention based on results of the electrodiagnostic testing.[2,3] Kim et al.[12] reported that the patient with traumatic facial nerve paralysis who had nerve conduction studies consistent with a poor prognosis regained considerable facial function after early surgical intervention; however, late exploration did not result in a positive outcome. Even though positive results have been reported in the literature with early surgery in selected cases, a recent systematic analysis revealed that the role of surgery versus nonsurgical interventions for this clinical entity remains inconclusive.[13] There were 7 (8.5%) CSF otorrhea cases in our research, 1 of which was seen with non-petrous fracture, and 6 of which were seen with petrous fractures. All of them were healed with conservative treatment (bed rest, head elevation, stool softeners, and prophylactic antibiotics). The reported incidence of CSF leak in temporal fractures ranges from 11%-45%.[3,7] In the diagnosis of CSF, the presence of a halo around the blood on the sponge is often suggestive. In suspected cases, the β2-transferrin test of the fluid is highly sensitive in identifying CSF leakage.[2] With the above-mentioned conservative measures, CSF leaks will generally heal in two weeks. CSF leaks that persist longer than 10-14 days most likely require surgical repair.[2,3] The use of prophylactic antibiotics remains controversial. However, in a meta-analysis, a significant increase in meningitis in patients who did not receive antibiotics was reported. Meningitis occurred in one of our patients who remained in the intensive care unit for a long time, but this patient did not have CSF leakage and healed with antibiotic treatment within three weeks. One of the most common findings of temporal bone fractures is blood otorrhea. These bleedings usually stop spontaneously. In cases of massive bleeding, a temporary pack is placed into the external auditory canal. This pack should be removed in 24 hours and a prophylactic antibiotic should be given. In cases in 428

which there is evidence of neurocranial injury on CT, angiography should be obtained in order to detect vascular injuries.[13] In conclusion, temporal bone fractures generally occur as a component of a severe head trauma, and traffic accidents are the most common etiologic factor. An otolaryngologist is an important part of the team together with the neurosurgeon who cares for patients with temporal bone fracture. The event starts with the first evaluation of the patient in the emergency department and may continue with follow-up and treatment of otolaryngologically important features, such as CSF fistula or facial nerve paralysis, repair of tympanic membrane, and management of hearing loss. In some cases, a prolonged follow-up, up to a year, may be required for the treatment and rehabilitation of patients.

REFERENCES 1. Işık HS, Bostancı U, Yıldız O, Ozdemir C, Gökyar A. Retrospective analysis of 954 adult patients with head injury: an epidemiological study. Ulus Travma Acil Cerrahi Derg 2011;17:46-50. 2. Gladwell M, Viozzi C. Temporal bone fractures: a review for the oral and maxillofacial surgeon. J Oral Maxillofac Surg 2008;66:513-22. 3. Johnson F, Semaan MT, Megerian CA. Temporal bone fracture: evaluation and management in the modern era. Otolaryngol Clin North Am 2008;41:597-618. 4. Yoganandan N, Baisden JL, Maiman DJ, Gennarelli TA, Guan Y, Pintar FA, et al. Severe-to-fatal head injuries in motor vehicle impacts. Accid Anal Prev 2010;42:1370-8. 5. Ahmed KA, Alison D, Whatley WS, Chandra RK. The role of angiography in managing patients with temporal bone fractures: a retrospective study of 64 cases. Ear Nose Throat J 2009;88:922-5. 6. Ishman SL, Friedland DR. Temporal bone fractures: traditional classification and clinical relevance. Laryngoscope 2004;114:1734-41. 7. Amin Z, Sayuti R, Kahairi A, Islah W, Ahmad R. Head injury with temporal bone fracture: one year review of case incidence, causes, clinical features and outcome. Med J Malaysia 2008;63:373-6. 8. Burgut HR, Bener A, Sidahmed H, Albuz R, Sanya R, Khan WA. Risk factors contributing to road traffic crashes in a fast-developing country: the neglected health problem. Ulus Travma Acil Cerrahi Derg 2010;16(6):497-502. 9. Hiroual M, Zougarhi A, El Ganouni NC, Essadki O, Ousehal A, Tijani Adil O, et al. High-resolution CT of temporal bone trauma: review of 38 cases. J Radiol 2010;91:53-8. 10. Saraiya PV, Aygun N. Temporal bone fractures. Emerg Radiol 2009;16:255-65. 11. Yetiser S, Hidir Y, Gonul E. Facial nerve problems and hearing loss in patients with temporal bone fractures: demographic data. J Trauma 2008;65:1314-20. 12. Kim J, Moon IS, Shim DB, Lee WS. The effect of surgical timing on functional outcomes of traumatic facial nerve paralysis. J Trauma 2010;68:924-9. 13. Nash JJ, Friedland DR, Boorsma KJ, Rhee JS. Management and outcomes of facial paralysis from intratemporal blunt trauma: a systematic review. Laryngoscope 2010;120:1397404. Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):429-435

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.86094

The mid-term results of treatment for tibial pilon fractures Tibia pilon kırıklarında orta dönem cerrahi sonuçlarımız Deniz GÜLABİ,1 Özgür TOPRAK,1 Cengiz ŞEN,2 Cem Coşkun AVCI,1 Erkal BİLEN,3 Fevzi SAĞLAM1

BACKGROUND

AMAÇ

In this report, the surgical treatment results of distal tibia (pilon) fractures are analyzed radiologically and clinically.

Bu yazıda, distal tibia (pilon) kırıklarının cerrahi tedavi sonuçları, radyolojik ve klinik olarak araştırıldı.

METHODS

GEREÇ VE YÖNTEM

Between 2002 and 2009, 32 feet of 31 patients (25 males, 6 females; mean age 46 years; range 17 to 72 years) who were treated surgically for tibial pilon fractures were evaluated. Open reduction and internal fixation were applied to 24 and external fixation to 8 fractures. The patients were evaluated according to the Teeny-Wiss functional ankle score, and overall assessment of reduction was calculated radiographically according to the criteria of Ovadia and Beals.

2002-2009 tarihleri arasında cerrahi olarak tedavi edilen 31 hastanın (25 erkek, 6 kadın; ortalama yaş 46; dağılım 17-72 yaş) 32 ayağı değerlendirildi. Bu kırıkların 24’üne açık redüksiyon ve internal fiksasyon, 8’ine eksternal fiksasyon yapıldı. Hastalar ortalama 46 ay takip edildi. Hastalar Teeny-Wiss fonksiyonel ayakbileği skorlamasına göre değerlendirildi. Radyolojik olarak kırık redüksiyon skorlaması Ovadia ve Beals kriterlerine göre yapıldı.

RESULTS

Tip 2 kırıkların 9’unda (%47,4), tip 1 kırıkların 5’inde (%26,3) ve tip 3 kırıkların 5’inde (%26,3) mükemmel sonuç elde edildi. Tip 3 kırıkların 9’unda (%69,2) kötü sonuç elde edilmişken, tip 1 ve tip 2 kırıkların 2’sinde (%15,4) kötü sonuç elde edildi. Eksternal fiksatör uygulaması ile karşılaştırıldığında, çok iyi ve iyi sonuçlar anlamlı derecede yüksek sayıda açık redüksiyon internal fiksasyon uygulaması ile elde edildi (sırasıyla, n=3, %15,8 ve n=16, %84,2; p<0.05).

While excellent results were achieved in 9 (47.4%) type 2, 5 type 1 (26.3%), and 5 (26.3%) type 3 fractures, fair/ poor outcomes were obtained in 9 (69.2%) type 3 and in 2 (15.4%) types 1 and 2 fractures each (p<0.015). Compared to the external fixation application, a statistically significantly higher number of excellent and good outcomes were obtained with open reduction internal fixation application (n=3, 15.8% vs n=16, 84.2%, respectively; p<0.05). CONCLUSION

BULGULAR

SONUÇ

If the principles of atraumatic soft tissue dissection, anatomic reduction of the joint face, stable fixation, and early mobilization of the patient are complied with in the surgical treatment of pilon fractures, successful results can be achieved. However, in type 3 fractures, even if these principles are complied with, post-traumatic arthritis is inevitable.

Pilon kırıklarının cerrahi tedavisinde, atravmatik yumuşak doku diseksiyonu, eklem yüzünün anatomik redüksiyonu, stabil bir tespit, erken hareket ve hastanın mobilizasyonu ilkelerine uyulduğunda başarılı sonuçlar alınabilmektedir, ancak bu prensiplere uyulmasına rağmen tip 3 kırıklarda travma sonrası artrit kaçınılmazdır.

Key Words: Rüedi-Allgöwer classification; surgical treatment; tibial pilon fractures.

Anahtar Sözcükler: Rüedi-Allgower sınıflaması; cerrahi tedavi; pilon tibia kırıkları.

1st Department of Orthopedics and Traumatology, Dr. Lütfi Kırdar Kartal Education and Research Hospital, Istanbul; 2Department of Orthopaedics and Traumatology, Bezmi Alem University, Istanbul; 3Department of Orthopaedics and Traumatology, Memorial Hospital, Istanbul, Turkey.

1 Dr. Lütfi Kırdar Kartal Eğitim ve Araştırma Hastanesi, 1. Ortopedi ve Travmatoloji Kliniği, İstanbul; 2Bezmi Alem Üniversitesi, Ortopedi ve Travmatoloji Kliniği, İstanbul; 3Memorial Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul.

1

Correspondence (İletişim): Deniz Gulabi, M.D. Caferağa Mah., Hacı Şükrü Sok., Sülün Apt. No: 11/9, Kadıköy, 34710 İstanbul, Turkey. Tel: +90 - 216 - 441 39 00 / 1351 e-mail (e-posta): dgulabi@yahoo.com

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Recently, the frequency of distal tibia intraarticular fractures has increased rapidly. A pilon fracture of the tibia involves the horizontal articular surface of the distal tibia with proximal extension. The main reasons are industrialization, prevalence of sports activities, and increase in domestic and traffic accidents. The pilon fracture is an intraarticular fracture of the lower end of the tibia and can be associated with various degrees of collapse and disintegration on the joint surface. One percent of lower extremity fractures and 7-10% of all tibia fractures are pilon fractures.[1-3] The usual mechanism of injury is axial loading of the limb through the ankle, with or without torsional load.[1,3,4] For the management of pilon fractures, various methods are recommended, such as manipulation and plaster application, external fixation, vertical transarticular and percutaneous pin fixation of large fragments and plaster application, stabilization of the fibula, open reduction and internal fixation (ORIF) to both tibia and fibula, primary arthrodesis, and even amputation. However, the most commonly used method is the ORIF approach.[2,4-6] External fixation of intraarticular fractures relies on distraction.[2] In the literature up to 1969, good results for pilon fractures were achieved in fewer than 50%. After Rüedi and Allgöwer introduced their open reduction techniques in 1969, they reported 71% good and excellent results for their four-year study. Heim and Naser[7] reported 90% good and excellent results in another study. The reason for the increase in good and excellent results is compliance to the ORIF principles introduced by Rüedi and Allgöwer. The operation consists of four surgical steps. 1-Reduction and fixation of the fibula, 2- Reconstruction and fixation of the tibia joint, 3-Filling of the metaphysical defect, which remains after the reconstruction of the joint, with autogenous spongious bone graft, and 4- Application of a support plate in order to prevent varus deformity, which might occur at a later stage.[2,8-14] In this study, the mid-term results of the ORIF method, which we applied to 31 patients with pilon tibia fractures, were evaluated in light of the literature.

MATERIALS AND METHODS Between 2002 and 2009, we studied 32 ankles of 31 patients (25 [81.25%] males, 6 [18.75%] females) in our clinic. Two senior attending surgeons treated all cases. Medical records, operative notes, and radiographs were reviewed by a surgeon not involved in the care of the patients. They had been operated with the established diagnosis of pilon tibia fracture and presented regularly for follow-ups. The extremity distribution of the cases was as follows: 19 right 430

Table 1. Distribution of accompanying injuries to pilon fractures Accompanying injuries Vertebra fracture Calcaneus fracture Scaphoid fracture Radius fracture Proximal tibia fracture Patella fracture Cuneiform fracture Fibula fracture

Case number 4 1 1 1 1 1 1 1

(61.3%), 11 left (35.4%) and 1 bilateral (3.3%). The youngest patient in our study population was 17 years old, and the oldest was 72 years old, with a mean age of 46 years. When the etiology of the traumas was considered, there were 18 (58%) falls from a height, 9 (29%) simple falls and 4 traffic accidents (13%). Thirteen of 32 patients with pilon fractures had open fractures. According to Gustilo-Anderson classification, our open fractures were of type 1 (n=3; 23%), type 2 (n=7; 53.9%), and type 3 (n=3; 23%), respectively. Twenty of our patients had 21 (65.6%) fibula lower end fractures. In 9 of our patients, there were 11 additional orthopedic pathologies (Table 1). For five of these accompanying additional pathologies (45%), a surgical operation was applied, and the rest (55%) received conservative treatment. Mean hospitalization period of our patients was 15.8 (5-44) days. In the preoperative evaluation, standard anteroposterior (AP) and lateral ankle radiographs and computerized tomographic (CT) images of the affected ankle were obtained. The fractures were categorized according to Rüedi-Allgöwer fracture classification. According to this classification, 7 type 1 (21.8%), 11 type 2 (34.2%) and 14 type 3 (44%) pilon fractures were treated. First, the skin condition of the patients hospitalized with a tibia pilon fracture was evaluated and their neurovascular examinations were made. Then, radiological examinations were performed. Skeleton traction from the calcaneus was applied to all patients with type 3 fractures, to 5 cases with type 2 and to 4 cases with type 1 fractures, and the affected ankles were supported with a Braun’s brace. Traction was not applied to the patients with minimal soft tissue damage; they were instead placed into a brace with ample cotton pad support, their affected knees were elevated, and ice compression was applied. In patients with open fractures, we applied debridement and serum isotonic irrigation in the operating room as soon as possible. We applied prophylaxis to prevent the development of tetanus and gaseous gangrene. For type 1 open fractures, we initiated treatment with a 1st genEylül - September 2012


The mid-term results of treatment for tibial pilon fractures

(a)

(b)

Fig. 1. (a) X-rays showing a comminuted tibial pilon fracture extending to the diaphysis in a 49-year-old man with type 3 fracture, who was operated on the 11th day postinjury. (b) X-rays of the same patient after internal fixation with the use of plate and screws.

eration cephalosporin (cephazolin sodium; 1g intravenous [iv]), while for type 3 open fractures, we started gentamicin (160 mg intramuscular [im] x 5 days) and metronidazole (500 mg iv x 3 days) therapy additionally. After regression of the foot and ankle edema and preoperative anesthesia examinations, the patients were taken to surgery. Mean time from the hospitalization to the operation was 10.7 days (1-28 days). For 32 pilon fractures, ORIF (n=24; 75%) and external fixation (n=8; 25%) were performed. Surgical Technique During the surgical procedures performed on 21 patients with a fibula fracture, firstly fibula fixation was applied to gain length according to the surgical technique suggested by Rüedi-Allgöwer. To fix the fibula, 1/3 tubular plate (n=9; 42.8%), intramedullary wire (n=8; 38.3%), dynamic compression (n=3; 14.2%), and semitubular plate (n=1; 4.7%) were used. ORIF was performed for tibias using an anterolateral (n=2), anteromedial (n=19), or short anterior (n=3) approach. The surgeons tried to leave at least 7 cm of healthy skin tissue between two incisions. After reconstruction of the tibia joint surface, osteosynthesis was applied using K-wires, cancellous screws or cannulated screws. Stabilization of 3 pilon fractures of 2 patients was achieved with these methods of osteosynthesis. In 21 fractures extending to the metaphysis, plates were applied because of inadequate fixation. For tibial fixations, a cloverleaf plate (n=2; 9.5%), or distal tibia lateral (n=2; 9.5%) or medial (n=17; 81%) compatible anatomic plates were used. Due to a metaphyseal defect, grafts were applied to 12 patients. After the scope examination of the fracture site, the previously applied tourniquet was opened, hemostatic controls Cilt - Vol. 18 Sayı - No. 5

were made, and a Hemovac drain was applied. The drain was removed on the 2nd postoperative day. The short leg brace was left in place. After postoperative regression of foot and ankle edema, active leg range of motion (ROM) exercises were started. In the 6th week, the patient was allowed to perform partial and at the end of the 3rd month full load-bearing exercises. External fixation was applied to 4 patients with second- and third-degree open fractures and to 4 patients whose comminuted fractures could not be fixed using internal fixation materials. The ankle joints of 6 of these patients were explored anteriorly with a 3 cm incision. For 4 patients, large fragments were reduced, fixed by means of K-wire, cannulated screws and spongious screws, and minimal osteosynthesis was applied. Afterwards, three pieces of 5 mm cortical nails were placed in the tibia and three pieces of 4 mm spongious nails in the calcaneus, and then an Orthofix type monolateral external fixator was applied. The other 2 patients were treated with the Ilizarov joint distraction method after fixation of the fibula without applying osteosynthesis to achieve the correct alignment. Before the surgery, all patients were given 1 g cephazolin iv injection. The same postoperative antibiotherapy was continued for 3 days as daily injections x3. After the first day of their hospitalizations, the patients received low molecular weight heparin (LMWH) prophylaxis until the 5th postoperative day. The patients managed with external fixation were mobilized with the aid of two crutches on the 1st day postoperatively. After documentation of radiological synostosis (approximately 16 weeks postoperatively), the fixator was removed and full load-bearing was allowed. The patients with a circular type fixator were mobilized on the 1st day postoperatively with full load-bearing status. 431


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(a)

(b)

Fig. 2. Clinical pictures of the same patient showing good ankle joint range of motion: dorsiflexion (a) and plantar flexion (b).

The foot rings of the patients were removed in approximately the 10th week postoperatively. The operated ankle was mobilized. At approximately the 16th week, after the observation of callus formation radiologically, the fixator was removed (Figs. 1a, b and 2a, b).

RESULTS The patients were evaluated according to the Teeny-Wiss ankle symptom and functional ankle scores. In this protocol, the evaluation was made by comparing the healthy ankle with a damaged ankle. According to these criteria, 32 pilon tibia fractures of 31 patients, who were monitored regularly, were evaluated. These patients were followed-up for an average of 46 months (8-97 months). In all of our patients, we achieved osseous union without a second intervention. The mean time to union was 16 weeks (10-25 weeks). According to the evaluation criteria, excellent (n=4; 12.5%), good (n=15; 46.8%), fair (n=6; 18.9%), and poor (n=7; 21.8%) outcomes were obtained. The radiographs obtained at the last follow-up were reviewed for union, loss of fixation, malunion, nonunion, and also for the quality of reduction according to Ovadia and Beals criteria. The results are listed in Table 2. Table 2. The mid-term results of the treatment for tibial pilon fractures

Quality of reduction by fracture type

Fracture Patient type no

Anatomic

Good

Fair

Poor

0 4 0 5 0 0

1 2 2 4 2 7

0 0 0 0 2 2

0 0 0 0 1 0

1 EF 1 ORIF 2 EF 2 ORIF 3 EF 3 ORIF

1 6 2 9 5 9

EF: External fixation; ORIF: Open reduction and internal fixation.

432

We did not detect any inadequacy of fixing material as a complication in our patients. No case of pseudoarthrosis or varus collapse was seen in any of our patients. Skin necrosis developed on the postoperative wounds of 1 case with a closed Rüedi-Allgöwer type 1 fracture and 1 case with Rüedi-Allgöwer type 3 and Gustilo-Anderson type 2 open fractures. These skin wounds were treated and healed with local dressing without the necessity of surgical intervention. In 4 of our patients, an infection developed on the postoperative wound. Three of these 4 patients with superficial infections had type 2 and 1 of them had type 3 open fractures. These patients were treated and healed with surface wound treatment and antibiotherapy without the necessity of a revision operation. In 1 patient, a deep infection developed at a later stage. This patient had Rüedi-Allgöwer type 3 and Gustilo-Anderson type 1 open fracture. The fixing material was extracted from the patient. Debridement and antibiotherapy were applied. The patient recovered without any sequela. Sudeck’s atrophy in 6 (18.75%), late-term synostosis in 3 (9%), and post-traumatic arthrosis in 7 (21.8%) of our patients developed postoperatively. Our patients with Sudeck’s atrophy healed using physiotherapy. Those with post-traumatic arthritis were monitored and informed about arthrodesis later. However, no additional surgery was performed in any of our patients.

DISCUSSION Pilon fractures generally occur after high energy traumas, and significant soft tissue injury is frequently present.[1-3] For these fractures, the severity of the trauma, inadequacy of local blood circulation, frequency of complications, and the high risk of becoming disabled have to be considered.[1,2,6] Etter and Ganz[15] studied 41 patients with pilon fractures, and stated that sport traumas are the most common etiologic factor. In his series with 42 patients, Bourne[16] found that the main etiologic factors are falling from a height, followed by motor vehicle Eylül - September 2012


The mid-term results of treatment for tibial pilon fractures

accidents. Ayeni[17] reported falling from heights, then simple falling, and thirdly traffic accidents as the main causes of pilon fractures. Heim and Nasser obtained 90% good results for patients with low energy traumas caused mostly by ski injuries. These types of traumas required ORIF. They had reported that the severity of the initial traumatic episode has a significant influence on the prognosis. [2,18] In the etiologic analysis of the 32 pilon fractures we treated, we saw a parallel with the Ayeni series. We obtained poor treatment outcomes in cases with high energy traumas, which were proportional to the severity of the trauma, soft tissue damage and patient demographics. In our series, there were no cases of pilon fractures secondary to ski injuries as was the case in the Rüedi series. The type of the fracture (open or closed) also affected the outcomes. In open fractures, the general approach to the management consists of debridement, irrigation and external fixator application.[19-22] For our patients with type 3 (n=2) and 2 (n=2) open fractures, we applied debridement, irrigation and an external fixator. We treated the remaining 9 patients with open fractures using secondary irrigation, debridement and then ORIF, as the soft tissue was suitable for this approach. These patients had type 3 (n=1), 1 (n=3), and 2 (n=5) open fractures. The Teeny-Wiss ankle symptom and functional scores of patients with type 1 open fractures were good while those of the patients who were operated due to types 2 and 3 open fractures indicated fair outcomes. The Teeny-Wiss ankle scores in 2 of our patients, who were treated with an external fixator due to type 3 open fractures, were indicative of poor outcomes. In one of those patients, superficial wound infection and degenerative arthritis developed during the postoperative period. The superficial wound infection was healed with antibiotherapy and dressing. For the treatment of degenerative arthritis, glucosamine was given and the patient was monitored. The patient was informed about the fact that arthrodesis may be necessary in the future. The Teeny-Wiss scores of 2 of our patients, who were treated with an external fixator because of type 2 open fractures, were suggestive of fair outcomes. Surface wound infection also developed in these patients, and healed with dressing and antibiotherapy. The aim in pilon fractures is to ensure a stable fixation after anatomical restoration of the injured joint and to initiate active movement of the ankle as soon as possible, while load is applied at a later time; however, this is not always possible. Primarily due to the soft tissue damage that also occurs because of the extreme trauma and defect in the joint and metaphysis, a stable osteosynthesis cannot be performed. Cilt - Vol. 18 Sayı - No. 5

The timing of the surgery in pilon fractures has always been a matter of debate. Early surgery should be applied within the first 8 to 12 hours. Rüedi-Allgöwer applied early surgery for the injuries in their series, which were mostly ski injuries. Burn and colleagues applied late-term surgery (7-10 days after the incident) to their patients who had mostly high energy traumas. No significant difference between early and late surgical outcomes was found.[23-26] The most important factor that determines the timing of the surgery is the urgent operability of the fractures. For instance, in some cases, in order to prevent skin and wound problems, the patients are not operated within the first 8-12 hours, and the surgery should be postponed for 7-10 days. We did not apply early surgery to any of our patients. In 4 of our patients, superficial wound infection developed, and was healed with dressing and antibiotherapy. For a patient with type 3 fracture, a late-term deep infection developed. After fusion of the fracture, the plate was removed and the fracture healed after debridement and irrigation. In fractures of the distal tibia extending to the joint, where functional good results can only be achieved in 50-60% of the cases, the main treatment principles remain: anatomical open reduction and rigid internal fixation and early mobilization and principles of lateterm load-bearing of the AO/ASIF group.[5,28,29] When different series are examined, the success rate in type 1 and type 2 fractures is about 80%, while it is only 40-50% in type 3 fractures. According to the literature, the functional results depend on the type of the fracture, and as the fracture becomes more complex, the results will also worsen. In Bourne’s series with 50 patients, the results of the treatments based on principles of AO (Arbeitsgemeinschaft für Osteosythesefragen [Association for Internal Fixation Researches], which is an international organization that originated in Switzerland) were significantly good.[4,30] The Teeny-Wiss ankle symptom and functional score average of our type 1 patients was 87 (76-94), of type 2 patients was 85 (64-94) and of type 3 patients was 77.14 (64-96), respectively. The external fixation of pilon fractures was first combined with open reduction by Scheck in 1965, and he reported successful results. With external fixation, the goal is to obtain reduction by using the ligamentotaxis property. However, in type 3 fractures, open reduction and minimal internal fixation of the joint might be necessary. While in type 1 and type 2 fractures it is enough to include the tibia in the fixation procedure, in type 3 fractures, the joint has to be included as well.[22,31,32] Otherwise, prevention of early joint movement and unfavorable healing of the cartilage might be encountered. 433


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We evaluated 32 pilon fractures of 31 patients treated in our clinic. Twenty-three of the fractures (72%) were caused by high energy trauma. Thirty-two pilon fractures were evaluated as type 1 (n=7; 21.8%), 2 (n=11; 34.2%), and 3 (n=14; 44%), while 13 of them (40.3%) were open fractures. ORIF was applied to 24 fractures and external fixation to 8 fractures. Independent of the treatment type, the functional outcomes of 18 patients with type 1 and 2 fractures were rated as excellent and good (78%) and fair (22%). In 14 patients with type 3 fractures, excellent and good (36%) and fair and poor (64%) results were obtained. In our series, which is in line with the literature, we also determined that the success rate changes with the type of the fracture. We believe that we obtained relatively better results (66%) with the ORIF method in the management of pilon fractures. Pilon fractures are problematic fractures with high complication rates. The main factors that increase the complication rate and decrease the functional outcomes are the type of the fracture (open or closed), severity of soft tissue injury, location of the open and joint fractures, and severity of the trauma.[1,6,33] The complications we encountered in our series were post-traumatic degenerative arthritis (22%), reflex sympathic dystrophy (21%), surface wound infection (12.5%), late symphysis (9%), skin necrosis (6.25%), angulation (3%), and late infection (3%). Our results are in parallel with the literature findings. Late arthritic changes are among the most important complications seen after the surgery of pilon fractures. They depend on the type of fracture, joint cartilage damage, and the type of the trauma. Our patients with post-traumatic arthritis had types 1 (n=1), 2 (n=1), and 3 (n=5) fractures, respectively. In 5 of the 14 patients with type 3 fractures, post-traumatic arthritis developed. These results agree well with the literature findings. It is known that degenerative changes occur depending on the success of the reduction. However, the damage in the joint cartilage during the trauma can cause degenerative arthritis in the late period even if a successful anatomical reduction was achieved. To achieve successful results in the treatment of pilon fractures, a very good preoperative planning has to be made. Successful results can be achieved with atraumatic soft tissue dissection according to biological principles, anatomic restoration of the joint surface, if necessary, rigid fixation using a bone graft, movement of the ankle in the early postoperative period, and late-term load application. Especially in advanced type 3 fractures, where an anatomical joint reconstruction is impossible, and also in polytrauma434

tized patients, acceptable results can be achieved with an external fixator application. However, there is no single successful treatment method that can be applied to all pilon fractures. Each fracture has to be treated individually and a treatment in compliance with surgical principles has to be well-planned.

REFERENCES 1. Reid JS. Pilon fractures update. Current Orthopaedic Practice. 2009;20:527-33. 2. Scott AT, Owen JR, Khiatani V, Adelaar RS, Wayne JS. External fixation in the treatment of tibial pilon fractures: comparison of two frames in torsion. Foot Ankle Int 2007;28:823-30. 3. Sands A, Grujic L, Byck DC, Agel J, Benirschke S, Swiontkowski MF. Clinical and functional outcomes of internal fixation of displaced pilon fractures. Clin Orthop Relat Res 1998:131-7. 4. Bourne RB, Rorabeck CH, Macnab J. Intra-articular fractures of the distal tibia: the pilon fracture. J Trauma 1983;23:5916. 5. Mast JW, Spiegel PG, Pappas JN. Fractures of the tibial pilon. Clin Orthop Relat Res 1988:68-82. 6. Boraiah S, Kemp TJ, Erwteman A, Lucas PA, Asprinio DE. Outcome following open reduction and internal fixation of open pilon fractures. J Bone Joint Surg [Am] 2010;92:34652. 7. Finsen V, Saetermo R, Kibsgaard L, Farran K, Engebretsen L, Bolz KD, et al. Early postoperative weight-bearing and muscle activity in patients who have a fracture of the ankle. J Bone Joint Surg Am 1989;71:23-7. 8. Topliss CJ, Jackson M, Atkins RM. Anatomy of pilon fractures of the distal tibia. J Bone Joint Surg [Br] 2005;87:6927. 9. Giachino AA, Hammond DI. The relationship between oblique fractures of the medial malleolus and concomitant fractures of the anterolateral aspect of the tibial plafond. J Bone Joint Surg Am 1987;69:381-4. 10. Leonard M, Magill P, Khayyat G. Minimally-invasive treatment of high velocity intra-articular fractures of the distal tibia. Int Orthop 2009;33:1149-53. 11. Møller BN, Krebs B. Intra-articular fractures of the distal tibia. Acta Orthop Scand 1982;53:991-6. 12. Rhinelander FW. Tibial blood supply in relation to fracture healing. Clin Orthop Relat Res 1974:34-81. 13. Yorgancıgil ME, Baran A, Yıdız M, Aksu S, Gürbüz A. Pilon kırıklarının tedavisinde ARİF’nin yeri. Acta Orthop Traumatol Turc 1994;28:87-9. 14. Sirkin M, Sanders R, DiPasquale T, Herscovici D Jr. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma 2004;18:32-8. 15. Etter C, Ganz R. Long-term results of tibial plafond fractures treated with open reduction and internal fixation. Arch Orthop Trauma Surg 1991;110:277-83. 16. Bourne RB. Pylon fractures of the distal tibia. Clin Orthop Relat Res 1989:42-6. 17. Ayeni JP. Pilon fractures of the tibia: a study based on 19 cases. Injury 1988;19:109-14. 18. Bhattacharyya T, Crichlow R, Gobezie R, Kim E, Vrahas MS. Complications associated with the posterolateral approach for pilon fractures. J Orthop Trauma 2006;20:104-7. 19. Bone L, Stegemann P, McNamara K, Seibel R. External fixation of severely comminuted and open tibial pilon fractures. Eylül - September 2012


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Clin Orthop Relat Res 1993:101-7. 20. Laughlin RT, Calhoun JH. Ring fixators for reconstruction of traumatic disorders of the foot and ankle. Orthop Clin North Am 1995;26:287-94. 21. Leone VJ, Ruland RT, Meinhard BP. The management of the soft tissues in pilon fractures. Clin Orthop Relat Res 1993;:315-20. 22. Murphy CP, D’Ambrosia R, Dabezies EJ. The small pin circular fixator for distal tibial pilon fractures with soft tissue compromise. Orthopedics 1991;14:283-90. 23. Bone LB. Fractures of the tibial plafond. The pilon fracture. Orthop Clin North Am 1987;18:95-104. 24. Helfet DL, Koval K, Pappas J, Sanders RW, DiPasquale T. Intraarticular “pilon” fracture of the tibia. Clin Orthop Relat Res 1994:221-8. 25. Ovadia DN, Beals RK. Fractures of the tibial plafond. J Bone Joint Surg Am 1986;68:543-51. 26. Thordarson DB. Complications after treatment of tibial pilon fractures: prevention and management strategies. J Am Acad Orthop Surg 2000;8:253-65.

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27. Teeny SM, Wiss DA. Open reduction and internal fixation of tibial plafond fractures. Variables contributing to poor results and complications. Clin Orthop Relat Res 1993:108-17. 28. Rüedi T. Fractures of the lower end of the tibia into the ankle joint: results 9 years after open reduction and internal fixation. Injury 1973;5:130-4. 29. Rüedi TP, Allgöwer M. The operative treatment of intraarticular fractures of the lower end of the tibia. Clin Orthop Relat Res 1979:105-10. 30. Bourne RB. Pylon fractures of the distal tibia. Clin Orthop Relat Res 1989;240:42-6. 31. Kim HS, Jahng JS, Kim SS, Chun CH, Han HJ. Treatment of tibial pilon fractures using ring fixators and arthroscopy. Clin Orthop Relat Res 1997;334:244-50. 32. McDonald MG, Burgess RC, Bolano LE, Nicholls PJ. Ilizarov treatment of pilon fractures. Clin Orthop Relat Res 1996;325:232-8. 33. Watson JT, Moed BR, Karges DE, Cramer KE. Pilon fractures. Treatment protocol based on severity of soft tissue injury. Clin Orthop Relat Res 2000;(375):78-90.

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):436-440

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.98511

Early period psychiatric disorders following burn trauma and the importance of surgical factors in the etiology Yanık travması sonrası erken dönemde görülen psikolojik bozukluklar ve etyolojide cerrahi faktörlerin yeri Hakan YABANOĞLU,1 Mahmut Can YAĞMURDUR,1 Nilgün TAŞKINTUNA,2 Hamdi KARAKAYALI1 BACKGROUND

AMAÇ

We aimed to assess early period psychiatric disorders following burn trauma.

Yanık travması sonrasında erken dönemde ortaya çıkan psikiyatrik bozukluklar değerlendirildi.

METHODS

GEREÇ VE YÖNTEM

The files of 1369 patients who had burn trauma were analyzed retrospectively. Forty-five patients with the diagnosis of psychiatric disorder were assessed based on the variables of age, gender, presence of chronic diseases, psychiatric disorders prior to burn trauma, cause of the burn, burn percentage, degree of burn, additional trauma, number of surgeries, duration of hospitalization, extremity amputation, intubation status, psychiatric symptoms, post-trauma psychiatric disorders, and mortality. RESULTS

Yanık travmasına maruz kalan 1369 hastanın dosyası geriye dönük olarak incelendi. Psikiyatrik bozukluk saptanan 45 hasta yaş, cinsiyet, kronik hastalık, yanık öncesindeki psikiyatrik bozukluk, yanık nedeni, yanık yüzdesi, yanık derecesi, ek travma, ameliyat sayısı, hastanede kalış süresi, ekstremite amputasyonu, entübasyon durumu, psikiyatrik semptomlar, travma sonrası psikiyatrik bozukluk ve mortalite açısından değerlendirildi. BULGULAR

Forty-five patients developed psychiatric disorder in the early period following burn trauma. Of the 45 patients, 7 (15.5%) were female and 38 (84.5%) were male. The mean age was 32±14.3 years, burn percentage was 40.09±20.69%, number of operations was 2.95±1.75, and the total duration of hospitalization was 51.57±38.62 days. Twelve (26.6%) patients had post-traumatic stress disorder (PTSD), 11 (24.4%) had delirium, 8 (17.7%) had anxiety disorder, 7 (15.5%) had depression, 1 (2.2%) had abstinence syndrome, 1 (2.2%) had schizoaffective disorder, 2 (4.4%) had PTSD and depression, 2 (4.4%) had PTSD and delirium, and 1 (2.2%) had PTSD and anxiety disorder.

Yanık travması sonrası erken dönemde 45 hastada psikiyatrik bozukluk saptandı. Hastaların 7’si (%15,5) kadın, 38’i (%84,5) erkekti. Ortalama yaş 32±14,3 yıl, yanık yüzdesi %40,09±20,69, geçirilmiş ameliyat sayısı 2,95±1,75, hastanede kalış süresi 51.57±38.62 gün idi. Hastaların 12’sinde (%26,6) post travmatik stres bozukluğu (PTSD), 11’inde (%24,4) deliryum, 8’inde (%17,7) anksiyete bozukluğu, 7’sinde (%15,5) depresyon, 1’inde (%2,2) yoksunluk sendromu, 1’inde (%2.2) şizoaffektif bozukluk, 2’sinde (%4,4) PTSD ve depresyon, 2’sinde (%4,4) PTSD ve deliryum ve 1’inde (%2.2) PTSD ve anksiyete bozukluğu görüldü.

CONCLUSION

SONUÇ

Burn is a trauma that can be treated with a multidisciplinary approach.

Yanık multisipliner yaklaşımla tedavi edilebilen bir travmadır.

Key Words: Burns; early diagnosis; psychiatric disorder.

Anahtar Sözcükler: Yanık; erken tanı; psikiyatrik bozukluk.

Departments of 1General Surgery, 2Psychiatry, Baskent University Faculty of Medicine, Ankara, Turkey.

Başkent Üniversitesi Tıp Fakültesi, 1Genel Cerrahi Anabilim Dalı, 2 Psikiyatri Anabilim Dalı, Ankara.

Correspondence (İletişim): Hakan Yabanoğlu, M.D. General Tevfik Sağlam Cad., Esertepe Mah., Bağevi Sok., Emlakbank Konutları. A2 Blok, No: 21, Kat: 5. Etlik 06100 Ankara, Turkey. Tel: +90 - 312 - 322 54 69 e-mail (e-posta): drhyabanoglu@gmail.com

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Early period psychiatric disorders following burn trauma and the importance of surgical factors in the etiology

Burn is one of the most important physical and psychological traumas that an individual can experience in his life. Burn trauma carries high morbidity and mortality rates due to numerous causes such as hypovolemic shock, infection and concurrent additional traumas. Due to the social and psychological problems associated with burn trauma, it has gone beyond being solely a physical trauma and has evolved into a serious problem that has a significant influence on the individual’s life. Especially in recent years, there have been serious advancements in burn treatment due to the increased quality of medical care, development of broad-spectrum antibiotics that are also effective on burn infections, improved intensive care conditions for burn patients, increased experience among physicians and supportive health personnel in burn trauma, patient referrals, nutritional support, early debridement and grafting, tissue production, and multidisciplinary approaches. Mortality and morbidity rates due to burn complications have diminished with the advancements in burn treatment. Because of high mortality rates and high costs, the best treatment option in burn trauma is prevention. The increased lifespan of patients with burn traumas has increased the need for rehabilitation and psychosocial treatment options for burn.[1] In patients with burn trauma, the initial choice of treatment is local and systemic treatment of the burned tissue. However, during the prolonged treatment period, psychological factors will also appear to be influential on treatment. Especially in patients who are hospitalized for extended periods, who have undergone numerous operations, have severe pain during medical dressing, have permanent physical and functional tissue loss, and have permanent labor loss, treatment compliance would decrease over time. This underlines the importance of providing psychological support in addition to physical support to the patient. Prevalence of psychiatric disorders in burn patients is between 28-75%.[2,3] Psychological disorders observed most frequently during the early period following the burn trauma include acute stress reactions, anxiety disorder, depression, behavioral disorders, and delirium.[4] Psychological disorders observed in hospitalized patients depend on the events occurring both during the trauma itself and during treatment approaches. Physical and psychological trauma in these patients should be treated medically and surgically for a long period of time. If patients are only treated physically, physiological disorders can emerge during the late period of treatment and this may disturb the patient’s attendance and cooperation with therapy, causing an increment in the patient’s hospital stay, morbidity and mortality rates, and costs. The aim of this study was to diagnose and treat the psychological disorders in the early period of burn trauma in order to prevent later Cilt - Vol. 18 Sayı - No. 5

medical and sociological complications and to identify the surgical factors causing psychological disorders to emerge.

MATERIALS AND METHODS In this study, the files of 1369 patients who were hospitalized at the Burn Intensive Care Unit (ICU) of the Burn and Fire Incidents Institute of Ankara Başkent University between October 1997 and July 2011 were analyzed retrospectively for psychiatric disorders emerging in the first 15 days of hospitalization. Forty-five patients who were found to have psychiatric disorders were assessed based on the variables of psychiatric disorders prior to burn trauma, cause of the burn, burn percentage, degree of burn, additional trauma, number of surgeries, duration of hospitalization, extremity amputation, intubation status, psychiatric symptoms, post-trauma psychiatric disorders, and mortality. Surgical factors that might cause psychiatric disorders were studied. The Statistical Package for the Social Sciences (SPSS, version 11.5) software program was used for data analysis in a computer environment. RESULTS In this study, we analyzed retrospectively the case files of 1369 patients. As a result of the analysis, 45 (3.2%) patients had psychiatric disorder accompanying the burn trauma. Of the 45 patients, 7 (15.5%) were female and 38 (84.5%) were male. The average age of the patients was 32±14.3 (8-80) years, burn percentage was 40.09±20.69% (5-85), number of operations was 2.95±1.75 (0-9), and the total duration of hospitalization was 51.57±38.62 (2-180) days. Seventeen (37%) patients had only 2nd degree deep burn, 2 (4.4%) had only 3rd degree, and 26 (58%) had 2nd degree deep and 3rd degree burn. When the mechanism of burn was considered, 32 (71%) were flame burn, 11 (24%) were electricity burn and 2 (4.4%) were hot water scald burn (4.4%). With regard to chronic diseases, 1 patient had diabetes mellitus (DM), 1 had hypertension (HT), 1 had DM, HT and chronic obstructive lung disease, and 1 had epilepsy. Six (13.3%) patients underwent extremity amputation in addition to debridement and grafting. None of the patients had a history of additional traumas. Twelve (26.6%) patients were administered tracheal intubation at different times during their hospitalization. An analysis of the psychiatric diagnosis prior to the trauma revealed that 1 patient had alcohol addiction, 2 had depression, 1 had anxiety disorder, 1 had schizoaffective disorder, and 1 had hyperactivity disorder. Distribution of the patients’ demographic characteristics and the data obtained based on the process of burn formation are given in Table 1. An analysis of the psychiatric disorders in the early period after the burn trauma showed that 12 (26.6%) 437


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Table 1. Distribution of patients according to demographic characteristics and mechanism of burn

patient with major burns was reported as $200,000. The cost of the treatment of entire burn cases is18 billion dollars per year.[6]

Mechanism of burn

Having both serious physical and psychological implications, burn trauma brings about not only serious medical problems but serious psychological problems as well. With the advancement of medical services and rehabilitation services geared towards burn patients, survival rates have increased. All these developments have carried psychiatry to a new level with regard to a multidisciplinary approach to burn trauma. The medical and surgical treatment of the patient is no longer the ultimate goal and providing psychiatric support to the patient has become an indispensible part of treatment during both the hospitalization period and the patient’s social life after discharge from the hospital. Especially complaints of severe pain, repeated medical dressing procedures and operations during the hospitalization period, cosmetic anxieties, permanent loss of labor skills, permanent limitation or loss of mobility, communication disorder, and extended periods of hospitalization often manifest themselves as psychiatric disorders. Failure to detect and treat these psychiatric disorders in a timely manner would decrease the patient’s compliance with medical and surgical treatment. A review of the literature reveals that the studies conducted have focused in general on parameters such as the types and prevalence of psychiatric disorders, their short-term and long-term follow-up, pre-existing psychiatric disorders, and gender.[9-13] In this study, in addition to these variables, the authors have also focused on other factors that they believed might be influential in causing these disorders, such as burn percentage, degree of burn, the process of burn formation, intubation status, amputation, total number of operations, and duration of hospitalization. An analysis of the results reveals that the patients face a very serious trauma. A review of the files of all patients shows that burn percentage in the patient group for which consultation was requested (3.2%) was 40%, burn degree was at least 2nd degree deep burn, the average number of operations was 3, and the average hospitalization duration was 51 days. Intubation (26.6%) and amputation (13.3%) rates were found to be higher than those for the general patient population. All parameters analyzed indicated a more severe trauma than that observed in the general patient population. It is inevitable for such an intense physical trauma to have psychiatric outcomes in both the shortand long term. During this period of time, the important point is to utilize that time to ensure the least damage with the help of appropriate psychological support from the beginning of trauma and at all stages.

Number of patients Sex Number of amputated patients Number of intubated patients Number of patients with psychiatric disorders pre-trauma Most common psychiatric diagnosis

Electrical Flame Scald burns burns burns 11 11 M

32 25 M/7 F

2 2M

3

3

0

3

8

1

1

3

2

Delirium

PTSD

SD, WS

PTSD: Post-traumatic stress disorder; SD, WS: Schizoaffective disorder and withdrawal syndrome; M: Male; F: Female.

Table 2. General distribution of psychiatric disorders in the early period after burn Psychiatric diagnosis PTSD Delirium Anxiety disorder Depression PTSD + Depression PTSD + Delirium PTSD + Anxiety disorder Withdrawal syndrome Schizoaffective disorder

Number of patients 12 (26.6%) 11 (24.4%) 8 (17.7%) 7 (15.5%) 2 (4.4%) 2 (4.4%) 1 (2.2%) 1 (2.2%) 1 (2.2%)

PTSD: Post-traumatic stress disorder.

patients had post-traumatic stress disorder (PTSD), 11 (24.4%) had delirium, 8 had (17.7%) anxiety disorder, 7 (15.5%) had depression, 1 (2.2%) had abstinence syndrome, 1 (2.2%) had schizoaffective disorder, 2 (4.4%) had PTSD and depression, 2 (4.4%) had PTSD and delirium, and 1 (2.2%) had PTSD and anxiety disorder (Table 2). The most frequent psychiatric symptoms observed in patients included sleep disorder, agitation, and visual and auditory hallucinations. Two (4.4%) patients died due to sepsis and 1 patient (2.2%) due to pneumonia.

DISCUSSION Burn trauma, affecting the entire organism and causing pathophysiological and psychological disorders, must be evaluated comprehensively. Burns, causing mortality and morbidity, are serious problems for people and society. In advanced burn units, mortality in major burns is 5.6%, and in Turkey it is reported as 7.5%.[5-8] In the United States, treatment cost of a 438

Recently, there has been a rise in the number of studies assessing the psychological and mental status EylĂźl - September 2012


Early period psychiatric disorders following burn trauma and the importance of surgical factors in the etiology

of burn patients. Prevalence of psychiatric disorders in burn patients is between 28-75%.[2,3] In our study, this rate was found to be 3.2%. In fact, the number of patients treated at our burn ICU between 1997 and 2007 was 1167, and a psychiatric consultation was requested for only 24 of them (2.1%). Psychiatric consultation was requested for only 21 (10.3%) of the 202 patients treated between 2007 and 2011. And overall, consultation was requested for 45 (3.2%) of the 1396 patients. It is noteworthy that burn treatment has reached an advanced level owing to the developments in the medical and surgical fields and that survival rates have increased. These findings have motivated practitioners to evaluate the psychological aspects of the trauma and adopt a multidisciplinary approach to burn trauma. In our clinic, the number of burn trauma patients who go through psychiatric assessment also increases in parallel to our increased experience in this field. Nevertheless, this rate is far below that in the literature. One of the reasons for this is that around 30% of the patients in our burn ICU are pediatric patients. Among the other reasons are the facts that the number of burn ICUs in our country is limited, the number of patients referred to our center is high, and a portion of these patients had intubation, a high burn rate or mortality in the early period; thus, it was not possible to provide the required psychiatric support to these patients. In burn trauma, handled and treated by most surgeons as only physical trauma, it must be kept in mind that burn trauma also has social and psychological elements. The treatment process may be accelerated for both patient and physician with psychological support in the early period. By this process, mortality and morbidity of burn, a serious social trauma, will decrease. Especially for patients with major burns, psychological support must be applied routinely as a part of medical and surgical approaches. The most frequent psychiatric disorders observed in burn patients are PTSD (5-45%) and depression (13-23%).[4,10,14,15] While the rate of depression after the burn incident was 2.2-53% during the first month, this ratio was 13-34% during the 12th month. On the other hand, while the frequency of PTSD in the early period was 2.2-26%, this ratio was 13-45% during the 12th month.[16-21] Risk factors for depression include presence of depression prior to the burn incident, female gender and scars causing deformations in the face. Risk factors for PTSD include presence of depression prior to the burn incident, type and severity of the symptoms at the onset, presence of pain-related anxiety, and visibility of the burn scar.[22] In our study, 12 (26.6%) patients were found to have PTSD, 11 (24.4%) delirium and 7 (15.5%) depression. These findings were consistent with those in the literature. Cilt - Vol. 18 Say覺 - No. 5

Three of our patients diagnosed with depression were female, and only 1 patient was diagnosed with depression prior to the trauma. Of those patients with the diagnosis of PTSD, only 1 of them had anxiety disorder prior to the trauma. Burn rates of 12 patients who were diagnosed with PTSD were 20-85%. Of these patients, 4 had 2nd degree deep burn, 1 had 3rd degree burn and 9 had 2nd and 3rd degree burn. Overall, it was observed that the burn rates of patients are high and that the related pain symptoms are excessive. The most common psychiatric symptom observed in PTSD patients was sleep disorder. The studies reveal that people with personality disorders, depression and alcohol and substance addiction become subject to burn traumas more often than individuals in the general population. Probability of observing a psychiatric disorder in patients prior to the burn trauma is 28-78%.[2,3] Six (13.3%) of our patients were previously diagnosed with a psychiatric disorder. In another study, a psychiatric disorder was diagnosed in 38.9% of the patients following the burn trauma; however, it was also found that a psychiatric disorder caused by trauma was observed in only 27.8% of these patients and that other patients had psychiatric disorders prior to the trauma as well.[13] Problems related to patience compliance and cooperation are commonly observed during the hospitalization process of these patients. These problems delay physical recovery and prolong the hospitalization period.[4] Psychological problems experienced in the early period following the burn trauma include overstimulation or sub-threshold stimulation, delirium, confusion, communication disorder, and sleep disorder. In our study, the most frequently observed symptoms included sleep disorder, agitation, and visual and auditory hallucinations. The treatment process that is started following a burn trauma is one of the most painful and stressful experiences that a patient may experience. Medical interventions made during the treatment and aimed at helping the patient survive most often disregard the psychological support that should be given to the patient. Psychological disorders observed in patients are usually not limited to the hospitalization period and continue to be observed even many years after the treatment.[9,13] Regardless of how well the patients may be functionally and cosmetically, they should be provided psychiatric support in order to be able to adapt themselves to social life, regain their self-esteem and overcome the psychological effects of the trauma. The results and sequelae of burn trauma have a great importance both for the individual society. Burn causes functional losses and social and psychological problems in the early and late healing period. The best treatment of burn is prevention. Individuals and institutions must take good care of themselves and 439


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other individuals with respect to the prevention of burn. It must be kept in mind that burn is a preventable trauma; thus, effective burn prevention education programs must be developed or improved. In conclusion, burn is a trauma that can be treated with a multidisciplinary approach. Psychiatric consultation should be requested as soon as possible for patients who refer to the burn ICU and who have high burn percentages and degrees, are candidates for multiple surgery, have a history of psychiatric diseases, and have extended periods of hospitalization. Surgical and medical treatment by itself is not sufficient for the treatment of burn patients. Psychiatric problems experienced by patients both during and after the trauma should always be considered. Patients and their families should seek professional support from psychiatrists. This would both improve patient compliance and expedite the process for the patient to resume his/her social life. Surgeons who play an important role in the surgical and medical treatment of burn patients should keep in mind that these patients will require psychological support as well.

REFERENCES 1. Munster AM. Measurements of quality of life: then and now. Burns 1999;25:25-8. 2. Brezel BS, Kassenbrock JM, Stein JM. Burns in substance abusers and in neurologically and mentally impaired patients. J Burn Care Rehabil 1988;9:169-71. 3. Davidson TI, Brown LC. Self-inflicted burns: a 5-year retrospective study. Burns Incl Therm Inj 1985;11:157-60. 4. Patterson DR, Everett JJ, Bombardier CH, Questad KA, Lee VK, Marvin JA. Psychological effects of severe burn injuries. Psychol Bull 1993;113:362-78. 5. Monafo WW. Initial management of burns. N Engl J Med 1996;335:1581-6. 6. Patel PP, Vasquez SA, Granick MS, Rhee ST. Topical antimicrobials in pediatric burn wound management. J Craniofac Surg 2008;19:913-22. 7. O’Brien SP, Billmire DA. Prevention and management of outpatient pediatric burns. J Craniofac Surg 2008;19:1034-9. 8. Gomez M, Cartotto R, Knighton J, Smith K, Fish JS. Improved survival following thermal injury in adult patients treated at a

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regional burn center. J Burn Care Res 2008;29:130-7. 9. Palmu R, Suominen K, Vuola J, Isometsä E. Psychiatric consultation and care after acute burn injury: a 6-month naturalistic prospective study. Gen Hosp Psychiatry 2011;33:16-22. 10. Lu MK, Lin YS, Chou P, Tung TH. Post-traumatic stress disorder after severe burn in southern Taiwan. Burns 2007;33:649-52. 11. Ehde DM, Patterson DR, Wiechman SA, Wilson LG. Posttraumatic stress symptoms and distress following acute burn injury. Burns 1999;25:587-92. 12. Dyster-Aas J, Willebrand M, Wikehult B, Gerdin B, Ekselius L. Major depression and posttraumatic stress disorder symptoms following severe burn injury in relation to lifetime psychiatric morbidity. J Trauma 2008;64:1349-56. 13. Ter Smitten MH, de Graaf R, Van Loey NE. Prevalence and co-morbidity of psychiatric disorders 1-4 years after burn. Burns 2011;37:753-61. 14. Yu BH, Dimsdale JE. Posttraumatic stress disorder in patients with burn injuries. J Burn Care Rehabil 1999;20:42633. 15. Fauerbach JA, Lawrence JW, Munster AM, Palombo DA, Richter D. Prolonged adjustment difficulties among those with acute posttrauma distress following burn injury. J Behav Med 1999;22:359-78. 16. Tedstone JE, Tarrier N. An investigation of the prevalence of psychological morbidity in burn-injured patients. Burns 1997;23:550-4. 17. Wiechman SA, Ptacek JT, Patterson DR, Gibran NS, Engrav LE, Heimbach DM. Rates, trends, and severity of depression after burn injuries. J Burn Care Rehabil 2001;22:417-24. 18. Maes M, Mylle J, Delmeire L, Altamura C. Psychiatric morbidity and comorbidity following accidental man-made traumatic events: incidence and risk factors. Eur Arch Psychiatry Clin Neurosci 2000;250:156-62. 19. Van Loey NE, Maas CJ, Faber AW, Taal LA. Predictors of chronic posttraumatic stress symptoms following burn injury: results of a longitudinal study. J Trauma Stress 2003;16:3619. 20. Williams EE, Griffiths TA. Psychological consequences of burn injury. Burns 1991;17:478-80. 21. Difede J, Barocas D. Acute intrusive and avoidant PTSD symptoms as predictors of chronic PTSD following burn injury. J Trauma Stress 1999;12:363-9. 22. Çakır S, Kulaksızoğlu BI. Psychological support of burn injury patients and burn unit staff. Turkiye Klinikleri J Surg Med Sci 2007;3:116-20.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):441-445

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2012.93467

Penetran kardiyak yaralanmalar: 21 olgunun değerlendirilmesi Penetrating cardiac injuries: assessment of 21 patients Yüksel DERELİ,1 Ramis ÖZDEMİR,1 Musa AĞRIŞ,1 Murat ÖNCEL,2 Kemalettin HOŞGÖR,1 Ali Suat ÖZDİŞ1 AMAÇ

BACKGROUND

Penetran kardiyak yaralanmalar, ciddi klinik sonuçları sebebiyle yüksek mortalite oranına sahiptir. Bu çalışmanın amacı, hastanemizde penetran kardiyak yaralanma nedeniyle cerrahi tedavi uygulanan hastaların araştırılmasıdır.

Penetrating cardiac injuries carry high mortality rates due to serious clinical outcomes. This study was planned to investigate patients treated surgically in our hospital for penetrating cardiac injury.

GEREÇ VE YÖNTEM

METHODS

Bu yazıda, Şubat 2006 ve Ocak 2011 tarihleri arasında hastanemize penetran kalp yaralanması şikayeti ile başvuran 21 hasta (18 erkek, 3 kadın) geriye dönük olarak incelendi. Hastalar klinik bulgular, tedavi yöntemleri ve sonuçları açısından değerlendirildi.

In this article, we reviewed retrospectively 21 patients (18 male, 3 female) suffering from penetrating heart injuries who admitted to our hospital between February 2006 and January 2011. Patients were evaluated with respect to clinical findings, treatment methods and clinical outcomes.

BULGULAR

RESULTS

Olguların 19’u delici kesici alet, 2’si ateşli silah yaralanması şeklindeydi. Tüm olgulara acil cerrahi girişim uygulandı. Kardiyak yaralanma 13 olguda sağ ventrikül, 5 olguda sol ventrikül ve 3 olguda sağ atriyum yaralanmasını içeriyordu. Sol atriyum yaralanması gözlenmedi. Kardiyak yaralanmalar primer dikiş yöntemi ile onarıldı. Mortalite 6 olgu ile %28,6 olarak saptandı. SONUÇ

Penetran kardiyak yaralanmalar genellikle genç yaş grubunda görülmektedir. Erken transport, uygun resüsitasyon ve acil cerrahi tedavi penetran kalp yaralanması olan hastaların hayatta kalma oranını artıracaktır.

Among the patients, 19 cases were due to stab injury and 2 cases to gunshot injury. Emergent surgical interventions were performed in all patients. Cardiac injuries involved the right ventricle in 13 patients, left ventricle in 5 patients and right atrium in 3 patients. There was no left atrial injury. Cardiac injuries were repaired by primary suturing method. Mortality was determined in 6 patients (28.6%). CONCLUSION

Penetrating cardiac injuries are seen generally in young people. Early transport, proper resuscitation and emergent surgery treatment improved survival in patients who sustained penetrating cardiac injuries.

Anahtar Sözcükler: Acil cerrahi; kardiyak yaralanma; penetran travma.

Key Words: Urgent surgery; cardiac injury; penetrating trauma.

Penetran kardiyak yaralanmalar, genellikle kesici delici aletler veya ateşli silahlarla meydana gelen yaralanmalardır. Acil cerrahi girişim gerektiren travma olgularının %10,4’ünü toraks travması oluştururken, bunların %1’i kardiyak yaralanmalardır.[1] Diğer travmalara göre daha az görülmesine rağmen, yüksek

mortalitesi nedeniyle önemli yaralanmalardır. Penetran kalp yaralanmasında yaşamı tehdit eden unsurlar koroner arter yaralanması, kapak yaralanması ve kalpteki yaranın yeri ve büyüklüğüne bağlı olarak gelişebilecek hipovolemi veya kalp tamponadıdır.[2] Kardiyak yaralanmalarda hastaların kısa surede hastaneye nakli,

Numune Hastanesi, Kalp ve Damar Cerrahisi Kliniği, Konya; 2 Selçuk Üniversitesi, Göğüs Cerrahisi Kliniği, Konya.

1

Department of Cardiovasculer Surgery, Numune State Hospital, Konya; 2 Department of Thoracic Surgery, Selçuk University, Konya, Turkey.

1

İletişim (Correspondence): Dr. Yüksel Dereli. Numune Hastanesi Kalp Damar Cerrahisi Kliniği, Konya, Turkey. Tel: +90 - 332 - 235 45 00 e-posta (e-mail): yuxel.dereli@mynet.com

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erken tanı ve resüsitasyonu takiben cerrahi girişimin en kısa sürede yapılması hayat kurtarıcıdır. Bu çalışmada, hastanemize son 5 yıl içinde penetran kardiyak yaralanma ile başvuran 21 hasta etyoloji, klinik özellikler, cerrahi tedavi ve sonuçları açısından geriye dönük olarak değerlendirildi.

GEREÇ VE YÖNTEM Şubat 2006 ile Ocak 2011 tarihleri arasında penetran kalp yaralanması sebebiyle Numune Hastanesi Kalp ve Damar Cerrahisi Kliniğinde cerrahi girişim uygulanan 21 olgu geriye dönük olarak incelendi. Hastalar etyoloji, fizik muayene bulguları, kardiyak tutulum, tedavi yöntemleri ve sonuçları açısından değerlendirildi (Tablo 1). Akciğer dışında eşlik eden organ yaralanması olan, başvuru anında uygulanan resüsitasyona cevap vermeyip kaybedilen ve cerrahi girişim uygulanmayan hastalar çalışma dışı bırakılmıştır. Hastalar anamnez ve fiziksel inceleme sonrası vakit kaybedilmeden ameliyata alındı. Hemodinamik olarak stabil olan 3 hastada ilave valvüler veya septal patoloji varlığını araştırmak için transtorasik ekokardiyografi yapıldı. Tüm olgulara sol anterolateral torakotomi ile cerrahi girişim uygulandı. Perikart açılarak tamponad boşaltıldı. Kanama kontrol altına alındıktan sonra kardiyak yaralanmalar prolen dikişlerle primer olarak onarıldı. Tüm olgularda perikart distal ucunda bir miktar açıklık bırakılarak kapatıldı. Olguların tümüne göğüs cerrahisi uzmanları da eşlik etti ve kardiyak onarım sonrası, akciğer hasarı olan 7 olguda gerekli tedavi prosedürleri uygulandı. Toraksa dren konularak ameliyat tamamlandı ve hastalar yoğun bakım ünitesine alındı. Tablo 1. Hastaların özellikleri

Ortalama yaş (yıl) 32,19 (18-62) Cinsiyet Kadın Erkek Etyoloji Ateşli silah Kesici delici alet Klinik tablo İnstabil Stabil Etkilenen kardiyak bölge Sağ ventrikül Sol ventrikül Sağ atriyum Koroner arter yaralanması Mortalite oranı 442

Sayı (Oran)

3 (%14,3) 18 (%85,7) 2 (%9,5) 19 (%90,5) 18 (%85,7) 3 (%14,3) 13 (%61,9) 5 (%23,8) 3 (%14,3) 1 (%4,8) 6 (%28,6)

BULGULAR Hastaların ortalama yaşı 32,2 (dağılım, 18-62) olup, 18’i erkek, 3’ü ise kadın idi. Yaralanma 19 olguda delici kesici alet, 2 olguda ise ateşli silah yaralanmasına bağlı idi. Anamnez bilgilerine göre hastaların hastaneye ulaşma süresi ortalama 25 (dağılım, 10-120) dakika idi. Beş hasta kendi özel araçları veya ticari araçlarla, diğer 16 hasta ise ambulans ile hastaneye getirilmişti. Üç hastada başvuru anında yaşam belirtisi yoktu ve resüsitasyon ile ameliyata alındı. On beş olgu hipovolemik şok ve tamponad tablosunda idi, 10 olgunun şuuru konfü, solunumu yüzeyel, hipotansif ve nabzı çok zayıf idi. Beş olgunun bilinci açık, hipotansif ve taşikardik idi. Diğer 3 olgu ise hemodinamik olarak daha stabil olup, sistolik arteriyel basınçları 80 mmHg’nın üzerinde ve nabızları dakikada 100’ün altında idi. Ameliyat sırasında kardiyak yaralanmanın 13 olguda sağ ventrikül, 5 olguda sol ventrikül ve 3 olguda sağ atriyumda olduğu gözlendi. Sol atriyumda yaralanma gözlenmedi. Sağ ventrikül yaralanması olan 2 olguda ön duvardaki kesinin tamir edilmesinden sonra kanamanın devam ettiği görüldü. Kontrolde bu olgularda ventrikülün arka duvarında da kesi tespit edildi ve primer dikişlerle posterior duvar da onarıldı. Sağ ventrikül yaralanması olan bir olguda, sağ koroner arter yaralanması da vardı. Bu olguda ventrikül yaralanmasının tamirinden sonra çalışan kalpte, safenvengrefti ile baypas uygulandı. Ateşli silah yaralanması ile başvuran 2 olguda ameliyat sırasında kardiyak arrest gelişti. Bu hastalarda sol ventrikülde geniş giriş ve çıkış yeri lezyonları gözlendi. Uygulanan internal kardiyak masaj ve ilaç tedavisine cevap alınamadı ve bu hastalar kaybedildi. Ateşli silah yaralanması etyolojisi olan ve resüsitasyon ile ameliyata alınan 2 hastada, masif kanama nedeniyle intraoperatif dönemde tekrar kardiyak arrest gelişti. Uygulanan internal kardiyak masaja ve medikal resüsitasyona cevap alınamadı ve bu hastalar kaybedildi. Ameliyattan sonra 1 hasta multipl kan transfüzyonuna bağlı yaygın damar içi pıhtılaşma (DIC), 2 hasta çoklu organ yetmezliği (MOF) ve ciddi akciğer yaralanması olan 1 hasta ise enfeksiyon nedeniyle kaybedildi. Toplamda 6 hasta kaybedildi ve mortalite %28,6 olarak tespit edildi. Diğer hastalar ortalama 2,5 (1-7) gün yoğun bakım ünitesinde takip edildi, drenleri alındıktan ve hemodinamik tabloları stabil hale geldikten sonra servise alındı. Bu hastaların postoperatif yoğun bakım ve klinik takibinde ilave komplikasyon gözlenmedi ve genellikle ameliyat sonrası 7’inci (513) günde şifa ile taburcu edildi. Hastalara taburculuk öncesinde ve ameliyat sonrası 1’inci aydaki kontrollerinde ekokardiyografi yapıldı ve patolojik bulgu saptanmadı.

TARTIŞMA Penetran kardiyak yaralanmalar sık görülmeyen, Eylül - September 2012


Penetran kardiyak yaralanmalar: 21 olgunun değerlendirilmesi

buna karşın mortalitesi oldukça yüksek olan travmalardır. Penetran toraks travmalarında kardiyak yaralanma oranı %10 civarında olmasına rağmen, toraks travması nedeniyle oluşan ölümlerin %40’ını kardiyak yaralanmalar oluşturmaktadır.[3] Çok sayıda olgu hastaneye ulaşmadan, olay yerinde hayatını kaybetmektedir. İlkyardım, iletişim ve transport alanındaki ilerlemelere paralel olarak hastaneye ulaştırılan ve tedavi edilen olgu sayısında artış gözlenmektedir. Penetran kardiyak yaralanmalar genç yaş grubunda ve erkeklerde daha sık görülmektedir.[1] Bizim çalışmamızda da ortalama yaş 32,19 (18-62) ve 21 olgunun 18’i (%85,7) erkek olup literatür verileri ile benzer idi. Penetran kardiyak yaralanmalarda mortalite ile ilgili olarak birçok çalışmada farklı oranlar verilmektedir. Mortalite, hastaneye ulaşana kadar geçen süre, etyoloji, etkilenen kardiyak bölge, lezyonun büyüklüğü, hastanın başvuru anındaki klinik tablosu, eşlik eden organ yaralanması, hastanenin imkanları ve ekibin deneyimine bağlı olarak değişmektedir.[4] Ateşli silah yaralanmalarında mortalite kesici delici alet yaralanmalarına göre daha yüksektir. Çünkü kardiyak dokularda daha geniş hasar meydana gelir, eşlik eden organ yaralanması daha sık görülür ve sonuçta bu hastalarhastaneye daha kötü klinik tablo ile başvurur.[5] Ateşli silah yaralanmasına bağlı kardiyak yaralanmalarda ortalama sağkalım %40 iken, kesici delici alet yaralanmalarında %80 olarak bildirilmektedir.[6] Çalışmamızda, ateşli silah yaralanmasına bağlı 2 olgu da kaybedilirken, kesici delici alet yaralanmasına bağlı olguların 4’ü kaybedildi ve toplamda 6 olgu ile mortalite %28,6 olarak saptandı. Penetran kardiyak yaralanmalarda hızlı transport hayat kurtarıcıdır. Hastaya ilk girişimi yapan ekibin tecrübe ve donanımı ile hastanın getirildiği acil servisin olanakları da mortalite üzerine etkili önemli faktörlerdir. Hastane öncesi önlemlerin de alındığı bir çalışmada mortalite oranının helikopter ambulansı ile hastaneye getirilen hastalarda %33, ambulansla getirilen hastalarda %76, niteliksiz araçlarla getirilen hastalarda %100 bulunduğu belirtilmektedir.[7] Buckman ve arkadaşları[5] tüm ölümlerin %78’inin kardiyak yaralanmadan sonraki ilk saatte oluştuğunu bildirmektedir. Bizim çalışmamızda, anamnez bilgilerine göre hastaların hastaneye ulaşım süresi 10 ile 120 dakika arasında değişiyordu. Olguların çoğunluğu ambulansla, bazı olgular ise kendi olanakları ile getirilmişti. Acil serviste hastayı gören hekimin kardiyak yaralanmadan şüphelenmesi erken tanı ve tedavi açısından önemlidir. Anatomik olarak prekordiyal bölgede; her iki meme başından geçen dikey çizgiler, sternal jugulum ve arkus kostarumdan geçen yatay çizgiler arasında görülen yaralanmalar aksi ispatlanıncaya kadar kardiyak yaralanma olarak değerlendirilmelidir.[8] Tanı Cilt - Vol. 18 Sayı - No. 5

için öykü ve fiziksel inceleme yeterlidir. Bu hastalarda ileri tanısal testler için genellikle zaman bulunamaz. Hemodinamik olarak stabil olan az sayıdaki hastada ekokardiyografi, bilgisayarlı tomografi gibi ileri tetkikler yapılabilir. Ekokardiyografi ile kardiyak yaralanma, tamponad, kapak ve septum hasarı hakkında bilgi edinilebilir.[9] Ancak stabil olmayan olgularda resüsitatif işlemlerin ardından acil operasyon uygulanmalıdır.[10] Özellikle agoni ve derin şoktaki hastalarda torakotominin geciktirilmesi mortalite oranını artırmaktadır.[8] Çalışmamızda hastaların büyük kısmı hemodinamik olarak instabil olup, fiziksel incelemenin ardından acil olarak ameliyata alındı. Klinik durumu stabil olan 3 hastada ameliyat öncesi transtorasik ekokardiyografik değerlendirme yapıldı. Kardiyak yaralanmalarda tamponadının mortaliteye etkisi için farklı görüşler mevcuttur. Genel olarak, tek bir kalp boşluğunu içeren ve özellikle sağ ventrikül yaralanmalarında tamponadın sağkalım üzerine olumlu etkisi olduğu kabul edilmekte, ancak bunun hangi mekanizma ile olduğu tam olarak bilinmemektedir.[11] Kesici delici alet yaralanmalarında %80-90 oranında perikardiyal tamponad oluşurken ateşli silah yaralanmalarında bu oran %20 kadardır.[6] Kesici delici aletlerle meydana gelen kardiyak yaralanmalarda mortalitenin ateşli silah yaralanmalarına göre daha düşük olması, daha yüksek oranda görülen tamponadın mortaliteye olumlu etkisi olduğu şeklinde yorumlanabilir. Bizim çalışmamızda hastaların 3’ü haricinde tamponad bulguları vardı, düşük mortalitede bunun da payı olabilir. Penetran kardiyak yaralanmada, anatomik lokalizasyonu itibarı ile en fazla sağ ventrikül yaralanması görülmekte ve bunu sırasıyla sol ventrikül, sağ atriyum ve sol atriyum izlemektedir.[10] Karrel ve arkadaşları penetran kardiyak yaralanmalarda kardiyak odacıkların tutulum oranlarını araştırdıkları çalışmalarında %42,5 sağ ventrikül, %33 sol ventrikül, %15,4 sağ atriyum ve %5,8 sol atriyum tutulumu tespit etmişlerdir.[12] Diğer yandan, sağ ventrikül yaralanmalarında mortalitenin daha düşük olduğu belirtilmektedir.[13] Çalışmamızda 13 olguda sağ ventrikül, 5 olguda sol ventrikül ve 3 olguda sağ atriyum yaralanması gözlendi, sol atriyum yaralanması gözlenmedi. Sağ kalım oranımızın yüksek olması, kısmen sağ ventrikül tutulumunun fazla olması ile ilgili olabilir. Penetran kardiyak yaralanmalarda koroner arter, kapak, septum ve diğer kardiyak yapılarda hasar gelişebilmekte ve bu durum mortaliteyi olumsuz etkilemektedir.[14] Bizim çalışmamızda 1 olguda sağ ventrikül yaralanması ile birlikte sağ koroner arter yaralanması gözlendi. Bu hastada kardiyak yaralanmanın tamirinden sonra çalışan kalpte, safen ven grefti ile sağ koroner artere baypas uygulandı ve hasta şifa ile taburcu edildi. Operasyon için seçilecek insizyon konusunda da 443


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farklı görüşler vardır. Hemodinamisi stabil olan olgularda median sternotomi tercih edilebilir. Çünkü mediansternotomi kalp, büyük damarlar ve hiler bölgenin değerlendirilmesi için çok iyi birgörüş alanı sağlar. [15] Ayrıca torakotomi ile karşılaştırıldığında solunum fonksiyonlarını daha az etkilemekte ve ağrı için daha az medikasyona ihtiyaç duyulmaktadır. Median sternotominin dezavantajı ise, kalbin posterioruna ve posterior mediasten yaralanmalarında aort ve özefagusa ulaşabilmek için uygun olmamasıdır.[15] Klinik durumu kritik olan hastalarda tercih edilecek yöntem acil departmanda uygulanacak anterolateral torakotomi olmalıdır ve sağ kalım oranlarında anlamlı artışla birlikte olduğu gösterilmiştir.[16] Sternotomiye göre daha hızlı uygulanabilir, gerektiğinde sternum kesilerek karşı hemitoraksa uzatılabilir.[8] Biz de çalışmamızda tüm hastalarda acil ameliyathanemizde sol anterolateral torakotomi uyguladık. Kardiyak yaralanmada onarım için primer dikişlerle, teflon veya perikart destekli dikişlerle ve gerektiğinde yama kullanılarak onarım önerilmektedir.[17] Kardiyak stabilite sağlandıktan sonra ilave yaralanma açısından tüm yapılar kontrol edilmelidir. Kardiyak yaralanmanın tamirinden sonra, oluşabilecek sızıntının toraksa sızması ve tekrar tamponada yol açmaması için perikardın distal ucunda küçük bir açıklık kalacak şekilde kapatılması uygun yaklaşım şeklidir. Kalbin onarımı sırasında ani kardiyak arrest gelişerek hastalar kaybedilebilir. Ani kardiyak arrest nedenleri arasında koroner arter yaralanması, aritmiler ve hava embolisi sayılabilir.[18] Çalışmamızda kardiyak yaralanma tüm olgularda primer dikiş tekniği ile onarıldı. Sağ ventrikül yaralanması olan 2 olguda ön duvardaki kesinin tamir edilmesinden sonra kanamanın devam ettiği görüldü. Kontrolde ventrikülün arka duvarında da kesi tespit edildi ve primer dikişlerle posterior duvar da onarıldı. Sağ ventrikül yaralanması olan bir olguda ilaveten sağ koroner arter yaralanması gözlendi ve kardiyak yaralanmanın tamirinden sonra çalışan kalpte, safen ven grefti ile baypas uygulandı. Ateşli silah yaralanması ile başvuran 2 olguda ameliyat sırasında kardiyak arrest gelişti. Bu hastalarda sol ventrikülde geniş giriş ve çıkış yeri lezyonları gözlendi. Uygulanan internal kardiyak masaj ve medikal tedaviye cevap alınamadı ve bu hastalar kaybedildi. Kardiyak yaralanmanın onarımını takiben koagulopati, sepsis, ensefalopati, mediastenit, yara yeri enfeksiyonu, pnömoni, rezidüel hematom ve postperikardiyotomi sendromu gibi ciddi ameliyat sonrası komplikasyonlar gelişebilir.[19] Koagülopati genellikle çok sayıdaki kan transfüzyonuna bağlıdır. Penetran kalp yaralanmasından sonra geç dönemde atriyal septal defekt, ventrikül septal defekti, valvüler yetmezlik, anevrizma formasyonu, iletim bozuklukları, ventriküler disfonksiyon, endokardit, perikardit ve 444

arteriovenöz fistül gibi komplikasyonlar görülebilir. [16] Çalışmamızda hastalar eksterne edilmeden önce ve ameliyat sonrası 1’inci ayda ekokardiyografi kontrolü yapıldı ve patolojik bulgu saptanmadı. Sonuç olarak, kardiyak yaralanmalar genç yaş grubunda daha sık görülen, ancak zamanında ve uygun tıbbi girişimle mortalitenin düşürülebileceği travmalardır. Sağ kalımın artırılması için, acil serviste oluşturulacak girişim odalarının tam donanımlı olması ve yardımcı sağlık personeline hizmet içi eğitim programları uygulanmasının önemli faktörler olduğu kanısındayız. KAYNAKLAR 1. Arikan S, Yücel AF, Kocakuşak A, Dadük Y, Adaş G, Onal MA. Retrospective analysis of the patients with penetrating cardiac trauma. Ulus Travma Acil Cerrahi Derg 2003;9:1248. 2. Mihmanlı M, Erzurumlu K, Türkay B, Kalyoncu A, Guney M. Penetran Kalp Yaralanmaları. Turkish J Thorac Cardiovasc Surg 1994;2:270-3. 3. Mandal AK, Oparah SS. Unusually low mortality of penetrating wounds of the chest. Twelve years’ experience. J Thorac Cardiovasc Surg 1989;97:119-25. 4. Kulshrestha P, Das B, Iyer KS, Sampath KA, Sharma ML, Rao IM, et al. Cardiac injuries-a clinical and autopsy profile. J Trauma 1990;30:203-7. 5. Buckman RF Jr, Badellino MM, Mauro LH, Asensio JA, Caputo C, Gass J, et al. Penetrating cardiac wounds: prospective study of factors influencing initial resuscitation. J Trauma 1993;34:717-27. 6. Attar S, Suter CM, Hankins JR, Sequeira A, McLaughlin JS. Penetrating cardiac injuries. Ann Thorac Surg 1991;51:7116. 7. Naughton MJ, Brissie RM, Bessey PQ, McEachern MM, Donald JM Jr, Laws HL. Demography of penetrating cardiac trauma. Ann Surg 1989;209:676-83. 8. Gao JM, Gao YH, Wei GB, Liu GL, Tian XY, Hu P, Li CH. Penetrating cardiac wounds: principles for surgical management. World J Surg 2004;28:1025-9. 9. Meyer DM, Jessen ME, Grayburn PA. Use of echocardiography to detect occult cardiac injury after penetrating thoracic trauma: a prospective study. J Trauma 1995;39:902-9. 10. Ivatury RR, Nallathambi MN, Rohman M, Stahl WM. Penetrating cardiac trauma. Quantifying the severity of anatomic and physiologic injury. Ann Surg 1987;205:61-6. 11. Asensio JA, Berne JD, Demetriades D, Chan L, Murray J, Falabella A, et al. One hundred five penetrating cardiac injuries: a 2-year prospective evaluation. J Trauma 1998;44:1073-82. 12. Karrel R, Shaffer MA, Franaszek JB. Emergency diagnosis, resuscitation, and treatment of acute penetrating cardiac trauma. Ann Emerg Med 1982;11:504-17. 13. Çıkrıkçıoğlu M, Yağdı T, Posacıoğlu H, Özkısacık E, Çalkavur T, Atay Y ve ark. Penetran kalp yaralanmaları. Ulus Travma Derg 2000;6:189-92. 14. Campbell NC, Thomson SR, Muckart DJ, Meumann CM, Van Middelkoop I, Botha JB. Review of 1198 cases of penetrating cardiac trauma. Br J Surg 1997;84:1737-40. 15. Mitchell ME, Muakkassa FF, Poole GV, Rhodes RS, GrisEylül - September 2012


Penetran kardiyak yaralanmalar: 21 olgunun değerlendirilmesi

wold JA. Surgical approach of choice for penetrating cardiac wounds. J Trauma 1993;34:17-20. 16. Hardikar AA, Thakur SS, Karmarkar PS, Ambike VS, Kanetkar AV, Golhar KB. Penetrating cardiac injury due to ball pointpen. Asian Cardiovasc Thorac Ann 1999;7:158-60. 17. Hood RM, Boyd AD, Culliford AT. Toracic trauma. Philadel-

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phia: WB Saunders Company; 1989. p. 178. 18. Demetriades D. Cardiac penetrating injuries: personal experience of 45 cases. Br J Surg 1984;71:95-7. 19. Velmahos GC, Degiannis E, Souter I, Saadia R. Penetrating trauma to the heart: a relatively innocent injury. Surgery 1994;115:694-7.

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Ulus Travma Acil Cerrahi Derg 2012;18 (5):446-448

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2012.77609

A rare cause of small bowel obstruction in adults: persistent omphalomesenteric duct Erişkinlerde ince bağırsak tıkanıklığının nadir bir nedeni: Persistan omfalomezenterik kanal Ali GÜNER, Can KEÇE, Aydın BOZ, İzzettin KAHRAMAN, Erhan REİS Previous abdominal surgery is the most common cause of mechanical small bowel obstruction. However, in patients with no abdominal surgery history, it is difficult to diagnose and treat. Omphalomesenteric duct is a primitive embryonic structure of fetal development between the midgut and yolk sac. In some cases, it may persist and result in several complications, particularly in childhood. In adults, intestinal obstruction due to persistent omphalomesenteric duct is an extremely rare circumstance. We report a 42-year-old male patient presenting with omphalomesenteric duct remnant causing small bowel obstruction.

Mekanik ince bağırsak tıkanıklığının en sık nedeni önceden yapılmış karın ameliyatlarıdır. Buna karşın, karın ameliyatı hikayesi olmayan hastalarda tanı koyulması ve tedavi zordur. Omfalomezenterik kanal fetal gelişim sırasında midgut ile yolk kesesi arasında yer alan embriyonik bir yapıdır. Bazı kişilerde, varlığı sebat eder ve özellikle çocukluk yaşlarında bazı komplikasyonlara neden olur. Erişkinlerde ise omfalomesenterik kanalın sebat etmesine bağlı gelişen bağırsak tıkanıklığı oldukça nadir rastlanılan bir durumdur. Bu yazıda, omfalomezenterik kanal açıklığının devam etmesine bağlı bağırsak tıkanıklığı gelişmiş 42 yaşındaki erkek hasta sunuldu.

Key Words: Intestinal obstruction; persistent omphalomesenteric duct; small bowel.

Anahtar Sözcükler: Bağırsak tıkanıklığı; persistan omfalomezenterik kanal; ince bağırsak.

Omphalomesenteric duct (OMD) is an embryonic structure providing communication from the yolk sac to the midgut during fetal development.[1] Normally, it obliterates spontaneously and separates from the intestine between approximately the 5th and 9th weeks of gestation. Complete or partial failure of such closure may result in various lesions. While Meckel’s diverticulum is the most common of these residual structures (2% of the population), presence of only a fibrous cord between the small intestine and the surface of the umbilicus is the rare entity. While they may be asymptomatic, some symptoms can occur because of OMD, and most of these symptoms usually appear before the age of four years.[2] Intestinal obstruction in adults is an extremely rare clinical presentation.

CASE REPORT

In this report, we present a case of persistent OMD causing intestinal obstruction in an adult patient.

A 42-year-old man presented to our department with intermittent abdominal pain, nausea, vomiting, and abdominal distension for 24 hours. He defined the absence of gas and feces for 48 hours. Physical examination demonstrated a distended abdomen and mild tenderness. Hyperactive bowel sounds were heard on auscultation. The blood test revealed leukocyte level of 12000/mm3 and no other laboratory abnormality. Plain abdominal film showed dilated small bowel loops and air-fluid levels (Fig. 1). Ultrasound reported dilated small bowel loops filled with fluid. He had no medical history, no hernia and no history of previous abdominal operations. After conservative follow-up with restriction of oral intake, nasogastric suction and fluid resuscitation, there was no resolution of the obstruction. Therefore, the operative intervention was

Presented at the 17th Turkish National Surgical Congress (May 26-29, 2010, Antalya, Turkey).

17. Ulusal Türk Cerrahi Kongresi’nde sunulmuştur (26-29 Mayıs 2010, Antalya).

Department of General Surgery, Trabzon Numune Training and Research Hospital, Trabzon.

Trabzon Numune Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, Trabzon.

Correspondence (İletişim): Ali Güner, M.D. Trabzon Numune Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, 61010 Trabzon, Turkey. Tel: +90 - 462 - 230 61 09 / 1822 e-mail (e-posta): draliguner@yahoo.com

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A rare cause of small bowel obstruction in adults

pecially in adult patients, is extremely rare, with very few cases reported in the literature.[5-8] Immediate diagnosis and differential diagnosis of the condition are important for deciding the treatment to be applied. The appropriate treatment and timing of the surgery remain controversial. However, the initial therapy of the bowel obstruction is standard and independent of the etiology. Fluid and electrolyte replacement, restriction of oral intake, and nasogastric suction are the important aspects of supportive care of patients with intestinal obstruction.[4] Broad-spectrum antibiotics may be administered in some because of concerns that bacterial translocation may occur or as a prophylaxis for possible resection. However, there are no controlled data to support this antibiotherapy. We performed the initial therapy for small bowel obstruction and antibiotic was administered only as prophylactic before the surgery. Fig. 1. Plain film shows multiple loops of dilated small bowel and air-fluid levels.

decided and midline laparotomy was performed. During the exploration, a fibrotic band was identified between the antimesenteric border of the terminal ileum and the posterior wall of the umbilicus, causing small bowel volvulus (Fig. 2a). The band was resected without any bowel resection (Fig. 2b). The postoperative period was uneventful and the patient was discharged on the 6th day with full recovery. The pathologic evaluation was reported as fibrous tissue.

DISCUSSION Mechanical small bowel obstruction is the most frequently encountered surgical problem of the small intestine. Intraabdominal adhesions related to previous abdominal surgery account for up to 75% of the cases of small bowel obstruction. Less prevalent etiologies include hernias, neoplasms, and inflammatory processes such as Crohn’s disease or tuberculosis. [3,4] Intestinal obstruction due to persistent OMD, es-

(a)

Non-operative treatments are effective and safe methods, particularly for adhesive small bowel obstructions.[4,6] However, if there is no history of an abdominal operation and no resolution of the obstruction findings, greater caution is required. Immediate diagnosis is especially important for the dangerous form of the obstruction, closed loop type obstruction, in which a segment of intestine obstructed both distally and proximally leads to rapid rise in the luminal pressure, and progresses to strangulation.[9,10] Small bowel volvulus, such as in the presented case, is one of the causes of closed loop obstruction; therefore, early surgery prevented the strangulation of the intestinal loops. Omphalomesenteric duct or vitelline duct is the connection between the yolk sac and the primitive midgut. Under normal circumstances, the duct obliterates to a thin fibrous band and is absorbed spontaneously during the 5th to 9th weeks of gestation. The intestine resides free within the peritoneal cavity. Persistence of the duct may result in several anomalies of the OMD including a blind OMD (Meckel’s diver-

(b)

Fig. 2. (a) Intraoperative view of the OMD between the intestinal loops and the abdomen. (b) The view of the OMD after resection. Cilt - Vol. 18 SayÄą - No. 5

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ticulum), omphalomesenteric cyst (a central cystic dilatation in which the duct is closed at both ends but patent in its center), an umbilical-intestinal fistula resulting from the duct remaining patent throughout its length, umbilical polyp resulting from the persistence of the distal end of the OMD, and complete obliteration of the duct, resulting in a fibrous cord extending from the ileum to the umbilicus.[11] The most common presentation of a persistent duct (67%) is the Meckel’s diverticulum, found in approximately 2% of the population.[12] Other OMD remnants occur infrequently. Although they may be asymptomatic, common symptoms of OMD malformations include abdominal pain, intestinal bleeding, intestinal obstruction, infection of the cyst, umbilical drainage, and umbilical hernia, and all of these symptoms appear to be age-dependent, usually before the age of four years. Adult cases of OMD remnant other than Meckel’s diverticulum are extremely rare. Though surgical intervention is necessary for a symptom-producing OMD remnant, it is not required for asymptomatic subjects. Intestinal obstruction, one of the complications of OMD, occurs owing to many mechanisms including intussusception of the diverticulum and volvulus or internal herniation from a fibrous connection, as in our patient. It is difficult to understand the etiology of the obstruction without diagnostic laparotomy or laparoscopy. Abdominal plain radiographs and ultrasonography are non-specific for small bowel obstruction. Abdominal computerized tomography may be useful to show the band originating from the umbilicus and continuing between the small bowel loops, as reported before. [6] In our case, we did not use computerized tomography, and both the plain radiographs and the abdominal ultrasonography were non-diagnostic. However, diagnosis was possible during laparotomy. The surgical excision of the fibrotic band is sufficient therapy. If intestinal strangulation is present, intestinal resection should be considered. Other types of symptomatic persistent OMD require different approaches, such as open surgical excision or laparoscopic excision.[8,11,12] In conclusion, small bowel volvulus due to persis-

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tent OMD is a very rare cause of intestinal obstruction in adults. However, in patients without any previous abdominal surgery, a correct diagnosis becomes more important. The excision of the OMD remnant is an easy, safe and definitive therapy.

REFERENCES 1. Moore TC. Omphalomesenteric duct malformations. Semin Pediatr Surg 1996;5:116-23. 2. Vane DW, West KW, Grosfeld JL. Vitelline duct anomalies. Experience with 217 childhood cases. Arch Surg 1987;122:542-7. 3. Miller G, Boman J, Shrier I, Gordon PH. Etiology of small bowel obstruction. Am J Surg 2000;180:33-6. 4. Sarraf-Yazdi S, Shapiro ML. Small bowel obstruction: the eternal dilemma of when to intervene. Scand J Surg 2010;99:78-80. 5. Amendolara M, Pasquale S, Perri S, Carpentieri L, Errante D, Biasiato R. et al. Intestinal occlusion caused by persistent omphalomesenteric duct and Meckel’s diverticulum: report of 2 cases. Chir Ital 2003;55:591-5. [Abstract] 6. Markogiannakis H, Theodorou D, Toutouzas KG, Drimousis P, Panoussopoulos SG, Katsaragakis S. Persistent omphalomesenteric duct causing small bowel obstruction in an adult. World J Gastroenterol 2007;13:2258-60. 7. Herman M, Gryspeerdt S, Kerckhove D, Matthijs I, Lefere P. Small bowel obstruction due to a persistent omphalomesenteric duct. JBR-BTR 2005;88:175-7. 8. Bueno Lledó J, Serralta Serra A, Planeéis Roig M, Dobón Giménez F, Ibáñez Palacín F, Rodero Rodero R. Intestinal obstruction caused by omphalomesenteric duct remnant: usefulness of laparoscopy. Rev Esp Enferm Dig 2003;95:736-8, 733-5. 9. Makita O, Ikushima I, Matsumoto N, Arikawa K, Yamashita Y, Takahashi M. CT differentiation between necrotic and nonnecrotic small bowel in closed loop and strangulating obstruction. Abdom Imaging 1999;24:120-4. 10. Fan HP, Yang AD, Chang YJ, Juan CW, Wu HP. Clinical spectrum of internal hernia: a surgical emergency. Surg Today 2008;38:899-904. 11. Nursal TZ, Yildirim S, Tarim A, Noyan T. Laparoscopic resection of patent omphalomesenteric duct in an adult. Surg Endosc 2002;16:1638. 12. Sawada F, Yoshimura R, Ito K, Nakamura K, Nawata H, Mizumoto K, et al. Adult case of an omphalomesenteric cyst resected by laparoscopic-assisted surgery. World J Gastroenterol 2006;12:825-7.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery Case Report

Ulus Travma Acil Cerrahi Derg 2012;18 (5):449-452 Olgu Sunumu doi: 10.5505/tjtes.2012.88965

Spontaneous migration of a retained bullet within the brain: a case report Beyin içinde kalan kurşunun kendiliğinden yer değiştirmesi: Olgu sunumu Mehmet ARSLAN, Metehan ESEOĞLU, Burhan Oral GÜDÜ, İsmail DEMİR, Abdul Baki KOZAN

Gunshot injury to the head is usually mortal, and spontaneous migration of a retained bullet is rare. We report the case of a 23-year-old man with a spontaneously migrated bullet within the brain. Cranial computerized tomography (CT) indicated that the bullet was lodged deeply in the left parietal region. The patient was conscious and had right homonymous hemianopsia. The bullet was close to the vital structures and deep-seated; therefore, surgical intervention was not considered. Two months after the injury, repeat CT revealed that the bullet had migrated posteriorly and caudally due to gravitational factors. Management of the retained bullet was controversial. Removal of a deep-seated bullet may cause additional neurological deficit, but migration of a retained bullet may cause damage to vital structures, producing significant neurological damage. We proposed that the bullet in the brain should be removed if it could be reasonably accessed without causing additional neurological damage.

Başın kurşun yaralanmaları genellikle ölümcüldür ve beyin içinde kalan kurşunun kendiliğinden hareketi nadir bir durumdur. Bu olgu sunumunda, 23 yaşındaki erkek hastanın beyninde kendiliğinden hareket eden kurşun sunuldu. Beyin bilgisayarlı tomogafisi (BT) kurşunun sol parietal bölgede derin yerleşimli olduğunu gösterdi. Hastanın bilinci açıktı ve sağ homonium hemianopsi vardı. Kurşun, hayati yapılara yakın ve derin yerleşimliydi. Bu yüzden, cerrahi girişim düşünülmedi. İki ay sonra çekilen kontrol BT’sinde kurşunun yerçekimi etkisi ile kaudale ve posteriyora doğru yer değiştirdiği görüldü. Beyin içinde kalan kurşunun tedavisi tartışmalıdır. Derinde yerleşen kurşunu çıkarmak ek nörolojik hasara neden olabileceği gibi kalan kurşunun hareketi de hayati yapıların zarar görmesine neden olabilir.Sonuç olarak, ek nörolojik defisite neden olmayacak kolay ulaşılabilir kurşunların çıkarılmasını öneriyoruz.

Key Words: Brain injury; bullet; spontaneous migration.

Anahtar Sözcükler: Beyin yaralanması; kurşun; spontan hareket.

Gunshot head injuries are the most lethal types of the cranial traumas and they are usually mortal. The mortality rate has been reported as ranging from 5184%.[1] The velocity, distance of flight, refraction, caliber, trajectory, bullet migration, brain damage degree, and vascular injury are the factors that affect mortality. [2] One of the most important factors in the prognosis is the Glasgow Coma Scale (GCS) score of the patient at the time of the initial evaluation.[1] The frequency of gunshot injuries to the head is on the increase and it becomes an important public health problem. Migration of the retained bullet is rare, and has been reported to occur in 0.06-4.2% of cases.[3,4] Many cases of spontaneous migration have been reported in the brain and

spinal canal.[2,3,5-9] Treatment of gunshot injuries is still debatable. The neurological status at the time of entry and location of the bullet often dictate the decision regarding surgical removal.

Department of Neurosurgery, Yüzüncü Yıl University, Faculty of Medicine, Van, Turkey.

Yüzüncü Yıl Üniversitesi, Tıp Fakültesi, Nöroşirürji Anabilim Dalı, Van.

We report a case of spontaneous migration of a retained bullet by reviewing the relevant literature.

CASE REPORT A 23-year-old male admitted with firearm injury to his head. In his physical examination, there was a single entry wound situated on the left side of the occipital bone, about 2 cm left of the midline and approximately 2.5 cm above the superior nuchal line; the exit wound could not be found. Brain tissue was

Correspondence (İletişim): Mehmet Arslan, M.D. Yüzüncü Yıl Üniversitesi, Tıp Fakültesi, Nöroşirürji Anabilim Dalı, Van, Turkey. Tel: +90 - 432 - 215 04 70 / 6315 e-mail (e-posta): arslan2002@hotmail.com

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(a)

(b)

Fig. 1. (a) Initial CT showing deep-seated bullet in the left parietal region. (b) Initial CT scans using a bone algorithm. The bullet is located in the left parietal lobe.

seen through the open wound. In the first neurological examination, the patient was confused and GCS at the time of admission was 10 (E3V2M5). Pupils were equally reactive, and his vitals were stable. Cranial computerized tomography (CT) revealed a bone defect of 0.5 cm in the left occipital region and a metallic object located in the posterosuperior side of the left lateral ventricle’s occipital horn. The bullet had passed through the left occipital lobe. There was hemorrhage along its trajectory, but the metal artifacts obscured the

(a)

damage (Figs. 1a, b). The entry wound was debrided and sutured. The patient was treated conservatively with antibiotics, antiepileptics, and anti-edema drugs. Having recovered, repeated neurological examination revealed defect of the right visual fields of each eye (right homonymous hemianopsia). He was discharged from the hospital after seven days of observation. Two months later, repeat cranial CT demonstrated that the bullet was lying on the tentorium cerebelli near the midline in the posterior occipital region (Figs. 2a, b);

(b)

Fig. 2. (a) Axial CT scan after two months using a bone algorithm, demonstrating the new position of the bullet in the occipital region on the tentorium cerebelli. (b) Sagittal CT using a bone algorithm showing bullet migration to the occipital lobe on the tentorium cerebelli. 450

EylĂźl - September 2012


Spontaneous migration of a retained bullet within the brain

when compared to the initial CT, it was observed that the bullet had migrated. Surgical intervention was not considered, as the patient displayed no new neurological deficit during the follow-up.

DISCUSSION Migration of an intracranial bullet is a rare complication of gunshot injuries to the head. The time course for migration ranges from 2 days to 3 months.[2,7,10] The course of a ricochet bullet is different from migration movement of a retained bullet. A ricochet bullet changes its direction after hitting the wall of the cranium or spinal canal, whereas retained bullet migration may be affected by several factors, such as gravitational factors. A bullet always tends to migrate.[9,11] Various theories have been put forward regarding migration of the bullet. The movement of a bullet in the nervous system occurs mainly due to gravitational forces.[3] Gravitational force acting on the bullet, which is denser than the surrounding medium, has been suggested as a cause for migration caudally by the effect of gravity related to the position of the body, especially in the absence of significant cranial swelling.[7,10] Castillo-Rangel and Salvati[2,12] suggested that the ventricular system provides transport of the bullet from one area of the brain to another. Cerebrospinal fluid (CSF) flow and pulsation will facilitate the bullet’s movement within the ventricle. However, it is difficult to say whether or not the movement of the bullet in the brain parenchyma depends on brain pulsation. Bullets reaching the CSF may migrate to a distant part of the brain or the spinal canal through the CSF. Lang[2] noted an intraventricular bullet had migrated to the aqueduct of Sylvius, producing acute hydrocephalus. Increased intracranial pressure due to cerebral swelling has been reported as a cause that prevents migration by compressing the pathway in the brain parenchyma. In the early stage after injury, brain edema may not allow migration of the bullet. However, migration along the CSF can still occur even in increased intracranial pressure. Penetration of the bullet leads to destruction in the white matter part of the parenchyma. This type of migration has been attributed to cerebral softening secondary to edema and local tissue damage, specific gravity of the bullet and gravitational factors.[2] Bullets that cannot move within the brain after an initial movement are presumably walled off by gliosis and fibrotic scarring. These processes usually take from weeks to years.[2] The deformed or non-deformed state of the bullet is significant; migration of a deformed bullet may be difficult due to increased resistance of the brain parenchyma.[6] In our case, cranial CT taken two months after the injury revealed that the bullet had migrated towards the left posterior occipital lobe on the tentorium cerebelli when compared to the previous location, with caudal and posterior migration. In this Cilt - Vol. 18 SayĹ - No. 5

case, movement of the intracranial bullet was ascribed to the specific gravity of the bullet, brain softening with loss of tissue resistance, white matter devitalization, and gravitational factors; however, gravity appears to be the most important factor responsible for the migration of the bullet. The petrous ridge, tentorium cerebelli and falx are natural barriers preventing migration of the bullet;[9] therefore, we considered that the bullet could not migrate from the tentorium cerebelli to another part of the brain. The indications for removal of an intracranial retained bullet are controversial and present a dilemma to the neurosurgeon. The management of these injuries needs to be studied in detail during the treatment procedure. Ă–zkan and colleagues[9] advised that a bullet in the brain should be removed if it can be reasonably accessed and if it can be removed without causing additional neurological damage. Kumar et al.[5] reported that removal of the bullet should be done in patients undergoing surgery for evacuation of a hematoma if it is easily accessible and removal does not lead to further deterioration of the neurological status due to its proximity to vital structures. Fujimoto et al.[6] stated that presence of a retained bullet and bone fragments do not increase the rate of intracranial infection; therefore, in an effort to prevent infection, removal of the bullet is not necessary. Zafonte et al.[13] reported two cases with neurological deterioration from spontaneous migration of a bullet; postoperatively, the patients demonstrated significant functional recovery. The study of Fujimoto[6] noted that a bullet within the ventricular system should be removed because hydrocephalus can be caused by obstruction of the foramen of Monro or aqueduct of Sylvius; however, a bullet within the brain parenchyma should be removed only when it can be easily accessed. Intracranial retained bullets require neurological observation and serial CT because migration may result in additional neurological deficits, and removal of the migrated bullet is thus advisable. Surgery tends to achieve debridement of devitalized tissue, removal of bone fragments, hemostasis, dural closure, and suturation of the entrance and exit wounds. In addition, antiepileptic and anti-edema agents and antibiotics should be administered. It should be kept in mind that a retained bullet may cause potential complications, such as migration, abscess, ventriculitis, toxicity, epilepsy, and hydrocephalus, which warrant surgical intervention. However, removal of the bullet may cause iatrogenic damage to the brain parenchyma; therefore, if there is no evidence of infection or brain abscess formation or of additional neurological deficit during hospitalization, conservative management can be preferred. The decision of surgical treatment of a bullet injury is difficult if it is in close proximity to vital structures, since re451


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moval of the bullet may cause significant neurological damage; however, migration can lead to a worsening of the neurological status of the patient. Therefore, it was decided to treat the case conservatively since the bullet was close to optic radiation carrying visual information to the visual cortex and was also deepseated (in its first location). We assumed that the bullet on the tentorium cerebelli (second location) was fixed, and there was no new neurological deficit as a result of the bullet’s migration. Preoperative localization of the bullet is important for its safe removal. CT taken shortly before surgery will be helpful for surgically accessing the bullet. Intraoperative fluoroscopy should also be performed to localize the bullet accurately.[6] While plain X-rays are useful in demonstrating change in position, they are not sufficient for an accurate anatomical localization for the important operation. In conclusion, if the bullet is close to vital structures, surgical intervention may not be considered. It is also recommended that deep-seated bullets be left, as any attempt at removal may increase the risk of morbidity and mortality; however, it should be kept in mind that the migrated bullet may also cause damage to a vital structure, leading to significant neurological damage.

REFERENCES 1. Ozdemir M, Unlü A. Gunshot injuries due to celebratory gun shootings. Turk Neurosurg 2009;19:73-6. 2. Castillo-Rangel C, Reyes-Soto G, Mendizábal-Guerra R. Cranio-thoracic bullet migration over a period of 27 years:

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case report. Neurocirugia (Astur) 2010;21:326-9. 3. Farrugia A, Raul JS, Géraut A, Ludes B. Ricochet of a bullet in the spinal canal: a case report and review of the literature on bullet migration. J Forensic Sci 2010;55:1371-4. 4. Rapp LG, Arce CA, McKenzie R, Darmody WR, Guyot DR, Michael DB. Incidence of intracranial bullet fragment migration. Neurol Res 1999;21:475-80. 5. Kumar R, Garg P, Maurya V, Sahu RN, Mahapatra AK. Spontaneous bullet migration-uncommon sequelae of firearm injury to the brain. Ind J Neurotrauma 2008;5:119-21. 6. Fujimoto Y, Cabrera HT, Pahl FH, de Andrade AF, Marino JR. Spontaneous migration of a bullet in the cerebellum-case report. Neurol Med Chir (Tokyo) 2001;41:499-501. 7. Agrawal A, Pratap A, Rauniar RK, Kumar A, Nepal U. Intracranial ricocheting of bullet from anterior clinoid process. JNMA J Nepal Med Assoc 2008;47:145-6. 8. Young WF Jr, Katz MR, Rosenwasser RH. Spontaneous migration of an intracranial bullet into the cervical canal. South Med J 1993;86:557-9. 9. Ozkan U, Ozateş M, Kemaloğlu S, Güzel A. Spontaneous migration of a bullet into the brain. Clin Neurol Neurosurg 2006;108:573-5. 10. Arasil E, Taşçioğlu AO. Spontaneous migration of an intracranial bullet to the cervical spinal canal causing Lhermitte’s sign. Case report. J Neurosurg 1982;56:158-9. 11. Duman H, Ziyal IM, Canpolat A. Spontaneous subfalcial transcallosal migration of a missile to the contralateral hemisphere causing deterioration in neurological status-case report. Neurol Med Chir (Tokyo) 2002;42:332-3. 12. Salvati M, Cervoni L, Rocchi G, Rastelli E, Delfini R. Spontaneous movement of metallic foreign bodies. Case report. J Neurosurg Sci 1997;41:423-5. 13. Zafonte RD, Watanabe T, Mann NR. Moving bullet syndrome: a complication of penetrating head injury. Arch Phys Med Rehabil 1998;79:1469-72.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):453-454

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2012.08931

The hidden devil: unexpected retained knife in the chest wall Gizli şeytan: göğüs duvarı içinde beklenmedik biçimde kalmış bıçak Chi-chen CHANG,1 Hung-jung LIN,1 Ning-ping FOO,2 Kuo-tai CHEN1

We report a 52-year-old woman presenting with stab wounds on her back and upper extremities. A knife retained in her chest wall was not discovered in the emergency department. This case reminds us that an obvious foreign body can be missed even after obtaining a detailed history, complete physical examination and plain film. Particularly, a retained foreign body increases the risk of infection and may cause further internal organ injury. We suggest that patients undergo computed tomography (CT) scanning whenever a penetrating wound cannot be explored adequately or the trauma surgeons are unable to perform detailed examinations on the injured patients. The CT images could delineate the course and severity of the penetrating injury, and decrease the risk of a retained foreign body.

Bu yazıda, sırtında ve üst ekstremitelerinde bıçak yaralarıyla gelen 52 yaşında bir kadın olgu sunuldu. Göğüs duvarında kalmış bıçak acil servis bölümünde fark edilmemişti. Olgu bize, ayrıntılı hasta öyküsü, tam bir fiziksel inceleme ve düz film çekilmesine rağmen belirgin bir yabancı cismin gözden kaçabildiğini hatırlatmaktadır. Çıkartılmamış bir yabancı cisim enfeksiyon riskini arttırabileceği gibi ilerde iç organ hasarına neden olabilir. Penetran yara yeterince incelenemediğinde veya travma cerrahı yaralı hastalarda ayrıntılı inceleme yapamıyorsa hastaların bilgisayarlı tomografi taramasından geçmesini öneririz. Bilgisayarlı tomografi görüntüleri penetran yaralanmayı, şiddetini ve yabancı bir cisim riskini aydınlatabilir.

Key Words: Foreign body; imaging; penetrating chest trauma; stab wound.

Anahtar Sözcükler: Yabancı cisim; görüntüleme; penetran göğüs travması; bıçak yarası.

We report a case of a woman presenting with stab wounds on her back and upper extremities. Neither the patient herself nor the trauma surgeons discovered the retained knife in her wound until surgery. This report highlights the unpredictability of retained foreign body in patients with penetrating injury.

pneumothorax nor signs of pulmonary parenchymal injury (Fig. 1). Eight hours later, the patient was transferred to the operating room for wound debridement and suture. An 18-cm knife that had entered from the back was found retained in the chest wall (Fig. 2). The blade had penetrated the right diaphragm and lung. The knife was surgically withdrawn and the postoperative recovery was uneventful.

CASE REPORT An obese 52-year-old woman was taken to the emergency department by ambulance. She had suffered an assault with a knife to her back, elbow and hands. On admission, the patient was coherent but in hypovolemic state with a blood pressure of 61/50 mmHg, heart rate of 83 per minute and respiratory rate of 24 per minute. We covered the wounds and the bleeding was stopped shortly thereafter. After infusion of isotonic saline and blood, her blood pressure normalized. Chest roentgenogram revealed neither hemoDepartments of 1Emergency, 2Emergency Medicine, Chi-mei Medical Center, Liouying, Taiwan.

DISCUSSION A foreign body may be observed anywhere in the chest as a result of a traumatic event. Although there is usually evidence of penetrating thoracic wound, a retained foreign body may occur unexpectedly. Previous studies suggest that the trauma surgeons should pay attention to the clinical history and trauma mechanisms, as well as to the radiologic findings.[1,2] However, the retained foreign bodies may be small or radiolucent Chi-mei Tıp Merkezi, 1Acil Servis, 2Acil Tıp Kliniği, Liouying, Tayvan.

Correspondence (İletişim): Kuo-tai Chen, M.D. 901 Chung-Hwa Road, Yung Kang, Tainan 710, Taiwan. Tel: +0886-6-2812811 (ext. 57196) e-mail (e-posta): 890502@mail.chimei.org.tw

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Fig. 1. Chest roentgenogram of the patient. The straight radiopaque line in her right lower chest wall was interpreted as a wire of various monitors used in the emergency department.

in character and thus difficult to discover on the plain film. In addition, the foreign bodies may migrate away from the wounds due to the exerted force from the trauma or may be pushed by the contracture of the muscles surrounding the object; further, the foreign bodies may be overlooked or misinterpreted as objects outside the patient’s body.[2,3] In our case, the wound on the patient’s back was small and the knife had penetrated deep along the chest wall, which caused it to be missed upon exploration of the wound. In addition, the patient arrived in a state of shock; therefore, the wound was covered to stop the bleeding as soon as possible instead of ensuring that a cautious examination was performed. Further, the patient had thick subcutaneous soft tissue (body mass index: 30.4) and neither the patient herself nor the trauma surgeons discovered the retained foreign body during the physical examination. The position of the knife made it appear as a metal line on the plain film. All these factors contributed to missing the retained foreign body in this patient. A retained foreign body carries several risks to the patient. The implanted foreign bodies are highly susceptible to pyogenic infections, and the infections are resistant to antibiotic therapy before the foreign bodies are removed.[3] Aside from possible infections, the

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Fig. 2. The retained foreign body: an 18-cm knife.

foreign bodies may migrate and cause further damage to internal organs.[4] Thus, it is crucial to discover any retained foreign bodies in penetrating chest wounds. In addition to a detailed history of the trauma mechanisms and careful physical examination, imaging studies are useful tools to identify a retained foreign body. Therefore, we suggest that patients undergo computed tomography (CT) scanning whenever a penetrating wound cannot be explored adequately or the trauma surgeons are unable to perform a detailed examination of an injured patient. The CT images provide information about the course of the penetrating object, the involved organs and the severity of organ injuries.[1,2] Most importantly, the CT image helps the trauma surgeons discover the retained foreign bodies and arrange for their proper removal.[2,3,5]

REFERENCES 1. Demetriades D, Velmahos GC. Penetrating injuries of the chest: indications for operation. Scand J Surg 2002;91:41-5. 2. de Vries CS, Africa M, Gebremariam FA, van Rensburg JJ, Otto SF, Potgieter HF. Et al. The imaging of stab injuries. Acta Radiol 2010;51:92-106. 3. Kim TJ, Goo JM, Moon MH, Im JG, Kim MY. Foreign bodies in the chest: how come they are seen in adults? Korean J Radiol 2001;2:87-96. 4. Sokouti M, Montazeri V. Delayed massive hemoptysis 20 years after lung stabbing: an unusual presentation. Eur J Cardiothorac Surg 2007;32:679-81. 5. Kavanagh PV, Mason AC, Müller NL. Thoracic foreign bodies in adults. Clin Radiol 1999;54:353-60.

Eylül - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):455-457

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2012.77012

Bilateral simultaneous anterior obturator dislocation of the hip by an unusual mechanism - a case report Olağandışı bir mekanizmayla çift taraflı, eşzamanlı anterior obturator kalça çıkığı: Olgu sunumu Asif SULTAN,1 Tahir Ahmad DAR,1 Mohd Iqbal WANI,1 Mubashir Maqbool WANI,1 Samina SHAFI2

A case of bilateral simultaneous anterior dislocation of the hip in a 30-year-old female is presented herein. The patient was managed conservatively. Follow-up at two years showed excellent results with no signs of avascular necrosis. The cause and mechanism of injury are discussed, which are different from those of previously reported cases.

Otuz yaşında bir kadın hasta çift taraflı ve eşzamanlı olarak her iki kalça ekleminde anterior dislokasyonla başvurdu. Hasta konservatif yolla tedavi edildi. İki yıllık takip avasküler nekroz belirtileri olmaksızın mükemmel sonuçlar alındığını gösterdi. Yaralanmanın önceden bildirilen olgulardan farklı olan nedeni ve mekanizması tartışıldı.

Key Words: Avascular necrosis; bilateral anterior dislocation of the hip; traumatic; mechanism of injury.

Anahtar Sözcükler: Avasküler nekroz; bilateral anterior kalça çıkığı; travmatik; yaralanma mekanizması.

Bilateral anterior dislocation of the hip is very rare. Only a few cases have been reported previously.[1-12] The majority of these cases were either due to road traffic accidents[2-4,7-9] or high- impact trauma.[1,5,11,12]

Radiographs of the pelvis were taken, which showed bilateral anterior dislocation of the hip joints into the obturator foramen. No associated fracture was seen (Fig. 1). The dislocations were immediately reduced under general anesthesia without any difficulty by traction in the line of the deformity followed by gentle adduction and internal rotation, with the pelvis stabilized by an assistant. Both hips were clinically stable after the closed reduction, with no restriction of range of motion. Post-reduction radiographs showed concentric and congruent reduction of both hips.

We describe a case involving simultaneous bilateral traumatic anterior obturator type hip dislocation with a distinctly different cause and mechanism of injury.

CASE REPORT A 30-year-old female presented to our emergency department with a history of slipping in the bathroom. Both her legs had extended outwards, and her buttocks had hit the bathroom floor. She immediately experienced severe pain in both hips, which she was unable to move. She arrived in the emergency department within two hours of the injury. On physical examination, both hips were in flexion, abduction and external rotation. Passive and active movements were not possible in either hip. There were no neurovascular deficits in either of her lower limbs. There were no associated injuries, and she was hemodynamically stable. Department of Orthopaedics, Bone and Joint Hospital, Barzulla Srinagar; 2 Government Medical College, Srinagar, India.

1

Skin traction (below knee) was applied on both sides and the patient was kept on bed rest for three weeks with continuous traction, followed by a further three weeks on non-weight-bearing. Weight-bearing was started six weeks after the injury, with the patient returning to full activities at three months. At the two-year follow-up, the patient was painfree with full range of motion of both hips and had no radiographic signs of avascular necrosis of the femoral head (Fig. 2). Barzulla Kemik ve Eklem Hastanesi, Ortopedi Kliniği, Srinagar; 2 Devlet Tıp Koleji, Srinagar, Hindistan.

1

Correspondence (İletişim): Asif Sultan, M.D. Government Hospital for Bone and Joint Surgery, Barzulla 190005 Srinagar, India. Tel: +919 858814700 e-mail (e-posta): drasifsultan@yahoo.com

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Fig. 1. Anteroposterior radiograph of the pelvis showing bilateral anterior dislocation of the hip into the obturator foramen.

Fig. 2. At the two-year follow-up, anteroposterior radiograph of the pelvis showing both hip joints with no avascular changes.

DISCUSSION Dislocations of the hip are classified as anterior or posterior according to the position of the femoral head. Anterior dislocations have been further subclassified as superior, inferior, and luxatio erecta of hip, obturator and pubic type.[13,14] Anterior dislocations of the hip are less common than posterior type, comprising 10-15% of all hip dislocations,[15] and inferior dislocation is the most common type of anterior dislocation, comprising more than 70% of anterior dislocations. [13] The lower incidence of anterior dislocation may be due in part to the strong anterior capsule and Y-shaped ligament of Bigelow, which is a strong disincentive to anterior dislocation.[13]

tocks hitting the floor and acting as a force in this hip position, causing both hips to be dislocated anteriorly and inferiorly into the obturator foramen. To the best of our knowledge, this cause/mechanism of injury has not been reported previously.

Superior dislocation occurs when the hip is forced into abduction and external rotation with extension of the hip. Inferior dislocation occurs when the hip is forced into abduction and external rotation with flexion of the hip. Obturator-type dislocation occurs in forced abduction, external rotation and flexion of the hip, and the force applied in this position seems to be the most likely mechanism.[7,13] Road traffic accidents were the cause of bilateral anterior dislocations of the hip in the majority of cases[2-4,7-9] with dashboard impact, where sudden deceleration created the dislocating force. Other cases reported also had high-energy trauma in the forms of a collapsed roof falling on to the lower back,[1] during electroconvulsive therapy,[5] by a collapsed floor on to a lower flat,[11] and by a striking blow from a heavy object (weighing 600 lbs) over the buttocks area,[12] with both lower extremities fixed and both hips flexed, abducted and externally rotated. Our patient had slipped in the bathroom with both her lower limbs going into wide abduction, with external rotation and flexion at the hips and with her but456

All the cases of bilateral anterior dislocation of the hips reported previously were reduced by closed methods, including our case, except for one neglected case. [1] Dislocation of the hip is an orthopedic emergency. Early reduction of the dislocated joint is necessary to reduce the risk of avascular necrosis, which is seen in 0-5% if the hip is reduced in less than six hours after the injury versus in 50% if the hip is reduced more than six hours after the injury.[13,14] In our case, the reduction was done within three hours of the injury. Prompt and gentle reduction under suitable anesthesia is very important to avoid complications, and for all hip dislocations, the goal is to obtain a congruent and stable hip. Consent: The report has been published after obtaining the due consent of the patient.

REFERENCES 1. Aggarwal ND, Singh H. Unreduced anterior dislocation of the hip. Report of seven cases. J Bone Joint Surg Br 1967;49:288-92. 2. M’Bamali EI. Unusual traumatic anterior dislocation of the hip. Injury 1975;6:220-4. 3. Gibbs A. Bilateral obturator dislocation of the hip joint. Injury 1980;12:250-1. 4. Zamani MH, Saltzman DI. Bilateral traumatic anterior dislocation of the hip: case report. Clin Orthop Relat Res 1981:203-6. 5. Sethi TS, Mam MK, Kakroo RK. Bilateral traumatic anterior dislocation of the hip. J Trauma 1987;27:573-4. 6. Tezcan R, Erginer R, Babacan M. Bilateral traumatic anterior dislocation of the hip: brief report. J Bone Joint Surg Br 1988;70:148-9. Eylßl - September 2012


Bilateral simultaneous anterior obturator dislocation of the hip by an unusual mechanism

7. Endo S, Hoshi S, Takayama H, Kan E. Traumatic bilateral obturator dislocation of the hip joint. Injury 1991;22:232-3. 8. Terahata N, Matsui H, Makiyama N. Bilateral anterior dislocation of the hips. A case report. Int Orthop 1996;20:125-6. 9. Sneath RJ, Morgan NP. Bilateral traumatic anterior dislocation of the hip joint. J Accid Emerg Med 1997;14:391. 10. Duygulu F, Karaoglu S, Kabak S, Karahan OI. Bilateral obturator dislocation of the hip. Arch Orthop Trauma Surg 2003;123:36-8. 11. Domingo A, Segur JM, Saz L, Ramiro SG.Unusual traumatic anterior bilateral hip dislocation. J Orthop Surg Traumatol 2008;18:475-8.

Cilt - Vol. 18 Say覺 - No. 5

12. Chung KJ, Eom SW, Noh KC, Kim HK, Hwang JH, Yoon HS, et al. Bilateral traumatic anterior dislocation of the hip with an unstable lumbar burst fracture. Clin Orthop Surg 2009;1:114-7. 13. Phillips AM, Konchwalla A. The pathologic features and mechanism of traumatic dislocation of the hip. Clin Orthop Relat Res 2000;377:7-10. 14. Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res 1973;92:116-42. 15. DeLee JC, Evans JA, Thomas J. Anterior dislocation of the hip and associated femoral-head fractures. J Bone Joint Surg Am 1980;62:960-4.

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Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):458-460

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2012.80000

Emergency surgery due to go-kart injuries: report of two consecutive cases Go-kart yaralanmalarına bağlı acil cerrahi: Ardışık iki olgunun sunumu Kerim Bora YILMAZ, Melih AKINCI, Oskay KAYA, Hakan KULAÇOĞLU

Injury due to go-karting accidents is a new kind of surgical emergency in Turkey and may show variations between patients. There are special details as relate to the design of the vehicles and patient characteristics. We report two seriously injured patients as a result of two different go-kart accidents. Severe intraabdominal hemorrhage due to liver laceration was seen in one patient and mesenteric intestinal avulsion in the other. Both patients were treated surgically and discharged uneventfully.

Go-kart kazasına bağlı yaralanma Türkiye’de yeni bir acil cerrahi türüdür. Hastalara göre çok değişik şekillerde izlenebilirler. Araçların tasarımı ve hasta karakteristikleri arasında ince ayrıntılarlar vardır. Bu yazıda, iki farklı go-kart kazasında iki ciddi yaralanma olgusu sunuldu. Bu hastalarda karaciğer laserasyonu ve mezenterik intestinal avulsiyona bağlı şiddetli karın içi kanama izlendi. Hastalar cerrahi yöntemlerle tedavi edildi, problemsiz olarak taburcu edildiler.

Key Words: Emergent surgery; go-kart; trauma.

Anahtar Sözcükler: Acil cerrahi; go-kart; travma.

The first kart was built by Kurtis Kraft in Southern California in 1956. The sport has rapidly spread to other Western countries. Recently, go-karting has become an attractive part of amusement parks in developing countries as well. It is gaining in popularity in Turkey, especially among the young population including teenagers.

CASE REPORTS Case 1- Over a long vacation, a 16-year-old male was admitted to the emergency department with abdominal pain due to a high-speed frontal collision to the tires near a race course while go-karting. He reported that he was driving a 9 hp go-kart at a speed

of 60 km/h and was wearing a helmet. He had generalized abdominal pain and tenderness and left ankle pain, with moving restriction. He was conscious, oriented and cooperative. Arterial blood pressure was 100/60 mmHg and pulse rate was 74 per minute. White blood count was 13,960/mm3, hematocrit 42.5% and hemoglobin 14.5 g/dl. Alanine transaminase was 193 U/L and aspartate transaminase was 242 U/L. Other hematologic and biochemical parameters were normal, but microscopic hematuria was determined on urine analysis. The plain X-ray films of cranium-neck, chest, abdomen, and extremities were normal. Ultrasound revealed minimal free liquid in the hepatorenal fossa and also in the pelvic region, with the deepest vertical height determined as 5 cm. No disintegration of parenchymatous organs was observed. Computed tomography could not be done because of the patient’s allergy history. The lesion on the ankle was evaluated as a soft tissue injury and conservative treatment was offered by an orthopedist. The urologist, neurosurgeon and thoracic surgeon reported normal examination findings. Exploratory laparotomy was decided to

4th Department of General Surgery, Diskapi Training and Research Hospital, Ankara, Turkey.

Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, 4. Genel Cerrahi Kliniği, Ankara.

Proctor and Miller[1] first reported go-kart injuries from the United Kingdom in 1973. To date, there have been a limited number of reports about go-kart casualties in the literature.[1-8] We present herein two different cases admitted to the same hospital (a registered trauma center) within two days during a local holiday.

Correspondence (İletişim): Kerim Bora Yılmaz, M.D. Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, İrfan Baştuğ Cad., Ankara, Turkey. Tel: +90 - 312 - 596 20 00 e-mail (e-posta): borakerim@yahoo.com

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Emergency surgery due to go-kart injuries

determine the source of a possible hemorrhage. During the exploration under general anesthesia, approximately 300 ml of blood was aspirated and grade-1 liver laceration in segment 7-8 was observed. Hemostasis was obtained by surface suturing of the liver. He began oral feeding on the postoperative second day and abdominal drains were removed on the third day. Postoperative abdominal ultrasound revealed diffuse urinary bladder mucosal wall thickness. The urologist recommended conservative treatment and prophylaxis for the urinary infection. The patient was discharged on the postoperative eighth day. Case 2- The day after the first patient presented, a 32-year-old male was brought urgently to our emergency service after colliding with the guardrail and wall at high speed while go-karting. His history revealed that he was driving a go-kart at 40 km/h and wearing a helmet as a safety precaution. He was conscious, oriented and cooperative. He had generalized abdominal pain and tenderness in all quadrants. Other systems were normal. Arterial blood pressure was 90/50 mmHg and pulse rate 110 per minute. White blood count was 10,000/mm3, hematocrit 44.3% and hemoglobin 15 g/ dl. Other hematologic and biochemical parameters and urine analysis were normal. The plain radiographs of cranium-neck, chest, abdomen, and extremities were normal. Abdominal ultrasound revealed diffuse free liquid between the intestinal loops, but the integrity of parenchymatous organs was normal. Fresh blood was found on paracentesis. Computed tomography was not done because of the clear findings on ultrasound. During the surgical exploration, approximately 2000 ml of blood was seen and aspirated. There was also a 70 cm mesenteric intestinal avulsion 70 cm proximal from the ileocecal valve. This segment was resected and an end-to-end anastomosis was done with double layer sutures. Other parts of intra- and retroperitoneal spaces were normal. Three units of erythrocyte suspension and one unit of fresh frozen plasma were given in the Intensive Care Unit (ICU). The patient was consulted by a urologist, neurosurgeon, orthopedist, and thoracic surgeon. No additional advice was given. On the postoperative second day, the patient began oral feeding and was transported to a clinic. On the postoperative seventh day, his drains were removed, and he was discharged without complication.

DISCUSSION Go-karting is a variant of an open-wheel motor sport with small, open, four-wheeled vehicles called karts (or go-karts, gearbox/shifter karts) depending on the design. They are usually raced on scaled-down circuits. Indoor and outdoor go-karting tracks accommodate thousands of people. News regarding go-kart accidents can be seen frequently in newspapers, audiovisual media and the Internet; however, accidents Cilt - Vol. 18 Say覺 - No. 5

have been reported in biomedical journals rarely. Interestingly, the first scientific paper on this subject used a newspaper report from The Times, dated 14 September 1972.[1] It was reported from the Netherlands that approximately 600 patients were admitted to emergency departments annually after go-kart accidents, and 12 severely injured patients were treated at Erasmus MC over a six-year period.[2] The abdominal injury can be as severe as pancreatic fracture requiring pancreaticojejunostomy.[3] In fact, go-kart emergencies are not limited to traumatic injuries; acute cardiovascular events can be seen due to hazardous air pollutant levels within the facilities for indoor go-karting.[9] Go-kart accidents cause injuries of variable extent and outcome. Eker and colleagues[2] divided the trauma mechanism and related injuries into three main groups as direct trauma, high energetic deceleration trauma and acceleration/deceleration trauma. They described different kinds of fracture, contusion, abrasion, laceration, and burn wound in group 1, blunt abdominal or thoracic trauma and compression injury to lower extremities in group 2, and flexion/extension injury in group 3. Both of our patients can be included in group 2 according to this classification. Karts vary widely in speed and some can reach speeds exceeding 160 miles (260 km) per hour, but they generally may be limited to speeds of no more than 15 miles (24 km) per hour.[10] The chassis is made of a flexible steel tube because there is no suspension. Thus, it is strong enough not to break or give way on turn. Amusement park go-karts can be powered by 4-stroke engines or electric motors, while racing karts use small 2-stroke or 4-stroke engines. As opposed to other sports that involve motorized vehicles such as motocross or Formula 1, implementation of safety measures by manufacturers and managers of go-karting tracts is not mandatory in most cases.[2] However, driver equipment, such as seat belt, full-face helmet, driving suit, gloves, driving boots, rib protector, and neck collar, has been determined.[10] In Germany, guidelines for the security of indoor kart centers were worked out but they do not have any legal liability in the case of injury.[3] The lack of safety devices and the subjective inexperience make this sport a dangerous type of entertainment. The importance of seat belts was highlighted in an experimental test study including go-karts.[11] In Turkey, we observe generally that the drivers use only a helmet in amusement parks. It was mentioned that the safety helmet is a widely utilized safety measure, resulting in a relatively low incidence of head and neck injuries as compared with traffic accidents.[2] The mechanism of injury differs among cases; how459


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ever, the most prevalent mechanism is steering wheel trauma. This kind of trauma usually causes chest injuries in car accidents.[12] However, it was shown that steering wheel trauma can also cause abdominal damage.[13] The two cases in the present report had abdominal injuries due to steering wheel contact. Although go-kart accidents have been a recognized type of trauma in Western countries for years, this surgical emergency has become a problem in developing countries only recently. It is a somewhat low-velocity vehicular accident, but can cause serious trauma in places where the formal protective measures are still lacking. Both the customers and the personnel in charge of the facility should be aware of the potential hazards and comply with safety rules and equipment requirements.

REFERENCES 1. Miller SS, Proctor D. Go-kart injuries at a fairground. Br Med J 1973;3:685-6. 2. Eker HH, Van Lieshout EM, Den Hartog D, Schipper IB. Trauma mechanisms and injuries associated with go-karting. Open Orthop J 2010;4:107-10.

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3. Govaert MJ, Ponsen KJ, de Jonge L, de Wit LT, Obertop H. Fracture of the pancreas in two patients after a go-kart accident. HPB (Oxford) 2001;3:3-6. 4. Suddaby B, Sourbeer M. Go-kart trauma-the heart of the matter. Pediatr Nurs 2004;30:336-7. 5. Bley T, Gahr RH. Risks and injuries of go-karting. [Article in German] Zentralbl Chir 2002;127:523-6. [Abstract] 6. Freeman BJ, Feldman A, Mackinnon J. Go-kart injuries of the shoulder region. Injury 1994;25:555-7. 7. Youngson GG, Baker R. Go-kart injuries. Injury 1978;9:2125. 8. Heddle RM, Robb WA. Go-kart injuries of the urethra. J R Coll Surg Edinb 1974;19:310-2. 9. Kim T, Wagner J. PM2.5 and CO concentrations inside an indoor go-kart facility. J Occup Environ Hyg 2010;7:397406. 10. http://en.wikipedia.org/wiki/Kart_racing. 11. Streff FM, Geller ES. An experimental test of risk compensation: between-subject versus within-subject analyses. Accid Anal Prev 1988;20:277-87. 12. Santavirta S, Araj채rvi E. Ruptures of the heart in seatbelt wearers. J Trauma 1992;32:275-9. 13. Lau IV, Horsch JD, Viano DC, Andrzejak DV. Biomechanics of liver injury by steering wheel loading. J Trauma 1987;27:225-35.

Eyl체l - September 2012


Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (5):461-462

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2012.35033

Isolated basal ganglia hemorrhage due to blast injury Blastik yaralanmaya bağlı izole bilateral bazal ganglion kanaması Fuldem Mutlu AYGÜN,1 Murat Serhat AYGÜN,2 Mehmet Bülent ÖNAL,3 Osman Lütfi DEMİRCİ4

Bilateral traumatic hemorrhage of the basal ganglia is an extremely rare neuropathologic entity. Bilateral basal ganglia hemorrhage secondary to blast injury has not described before. We report a case with bilateral basal ganglia hemorrhage secondary to explotion.

Bilateral travmatik bazal ganglion kanaması son derece nadir bir nöropatolojik antitedir. Blastik yaralanmaya bağlı bilateral bazal ganglion kanaması daha öncesinde hiç tanımlanmamıştı. Patlamaya bağlı gelişmiş bilateral bazal ganglion kanaması olan bir olgu sunuldu.

Key Words: Basal ganglia; hemorrhage; trauma.

Anahtar Sözcükler: Basal ganglion; kanama; travma.

Bilateral basal ganglia hemorrhages are extremely rare and generally occur due to hypertension.[1] There are some reports about bilateral basal ganglia hemorrhage etiologies like lightening,[2] diabetic ketoacidosis,[3] and alcohol and cocaine intoxication,[4] but only a few articles about trauma.[5,6]

Conservative treatment was carried out, and the patient was discharged about seven days later without any deficit.

Non-contrast computed tomography (CT) was performed, and revealed bilateral basal ganglia hemorrhage with peripheral edema (Fig. 1), without any signs of subdural or subarachnoid bleeding.

DISCUSSION Blast injuries are divided into four classes: primary, secondary, tertiary, and quaternary. Primary injuries are caused by blast overpressure waves or shock waves. These are especially likely when a person is close to an explosion. The extent and types of primary blast-induced injuries depend on the peak of the overpressure, number of overpressure peaks, time lag between overpressure peaks, characteristics of the shear fronts between overpressure peaks, frequency resonance, and electromagnetic pulse. Researches have focused on the mechanisms of blast injuries within gascontaining organs/organ systems such as the lungs, while primary blast-induced traumatic brain injury has remained underestimated. Secondary injuries are due to bomb fragments, tertiary injuries are due to blast wind, and quaternary injuries include all other injuries

1 Department of Radiology, Siirt Obstetrics and Gynecology and Children Health Hospital, Siirt; Departments of 2Radiology, 3Neurosurgery, 4Emergency Medicine, Siirt State Hospital, Siirt, Turkey.

1 Siirt Kadın Doğum ve Çocuk Hastalıkları Hastanesi Radyoloji Bölümü, Siirt; Siirt Devlet Hastanesi, 2Radyoloji Bölümü, 3Beyin Cerrahisi Kliniği, 4 Acil Servis, Siirt.

We report herein a case of bilateral basal ganglia hemorrhage due to blast injury.

CASE REPORT A 35-year-old man was admitted to our clinic after injury due to a rocket explosion. Neurological examination revealed that the patient was comatose, and the physical examination revealed only a mild scalp laceration. Chest radiography, electrocardiogram, and blood pressure were all normal.

Correspondence (İletişim): Murat Serhat Aygün, M.D. Siirt Devlet Hastanesi, 56100 Siirt, Turkey. Tel: +90 - 484 - 223 10 21 e-mail (e-posta): drserhataygun@gmail.com

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injury) can explain the etiology, but it is possible that the sudden-onset hypertension due to the adrenaline discharge caused the bilateral basal ganglia hemorrhage. This topic requires further investigations about blast injury to understand the actual mechanism of blast bilateral basal ganglia hemorrhage. Computed tomography (CT) remains essential in blast trauma, as it shows injuries to the lung or other parenchymal organs. Likewise, cranial injury can be revealed with non-contrast cranial CT, and cranial examination should be performed in patients with blast injury. Bilateral basal ganglia hemorrhage must be documented as a complication of blast injury. In conclusion, researches about bilateral basal ganglia hemorrhage are needed in order to understand the mechanism of hemorrhage secondary to blast injury.

REFERENCES Fig. 1. Axial plane computed tomography shows bilateral basal ganglia hemorrhage (arrows) with mild edema.

not covered in the first three classes.[7] To our best knowledge, there are a few articles about traumatic bilateral basal ganglia hemorrhage, but none about blast injury.[5,6] The mechanism of traumatic basal ganglia hemorrhage has not been clear, but is believed to arise from a shear strain in the ganglionic region. Likewise, we could not determine the factors that led to the bilateral basal ganglia hemorrhage in our case. The high pressure of the blast injury (primary injury) or head trauma by blast wind (tertiary

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1. Weisberg LA, Stazio A, Elliott D, Shamsnia M. Putaminal hemorrhage: clinical-computed tomographic correlations. Neuroradiology 1990;32:200-6. 2. Ozgun B, Castillo M. Basal ganglia hemorrhage related to lightning strike. AJNR Am J Neuroradiol 1995;16:1370-1. 3. Cho SJ, Won TK, Hwang SJ, Kwon JH. Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome. Yonsei Med J 2002;43:533-5. 5. Renard D, Brunel H, Gaillard N. Bilateral haemorrhagic infarction of the globus pallidus after cocaine and alcohol intoxication. Acta Neurol Belg 2009;109:159-61. 6. Yanaka K, Egashira T, Maki Y, Takano S, Okazaki M, Matsumaru Y, et al. Bilateral traumatic hemorrhage in the basal ganglia: report of two cases. [Article in Japanese] No Shinkei Geka 1991;19:369-73. [Abstract] 7. Jang KJ, Jwa SC, Kim KH, Kang JK. Bilateral traumatic hemorrhage of the basal ganglia. J Korean Neurosurg Soc 2007;41:272-4.

Eyl端l - September 2012


Değerli Meslektaşlarım, Sizleri 19-23 Nisan 2013 tarihleri arasında Antalya’da gerçekleşecek olan 9. Ulusal Travma ve Acil Cerrahi Kongresi’ne davet etmekten mutluluk duyuyoruz. Bu kongrede, Travma ve Acil Cerrahi konusunda en üst düzeyde bilgi birikimi ve yoğun deneyimle elde edilebilecek, tanı, tedavi, organizasyon ve hasta bakımı alanındaki tüm gelişmeler bilgilerinize sunulacaktır. Kongre programı kongre öncesi kursları, uzman oturumları, video sunumları, interaktif paneller, tartışma oturumları, uzlaşma toplantıları, konferanslar ve uzmanlık alanındaki yenilikleri içermektedir. Hedefimiz değerli görüşlerinizle bilimsel programımızı zenginleştirip, herkesin birbirinden bir şeyler öğrenebileceği bilimsel bir platform gerçekleştirmektir. Antalya tarih boyunca kültürün, sanatın, mimarinin ve mitolojinin merkezi olmuştur. Muhteşem doğası, açık maviden laciverte uzanan denizi, şelaleleri, Toros dağları ve palmiye ağaçları ile bu gölgenin büyüsüne kapılacaksınız. Bu özellikleri ile de Antalya, Travma ve Acil Cerrahideki son gelişmeleri tartışabileceğimiz en uygun yer. Sizi Antalya’da ağırlamaktan büyük memnuniyet duyacağız. Saygılarımızla, Recep Güloğlu Salih Pekmezci Ulusal Travma ve Acil Cerrahi Derneği Başkanı Kongre Başkanı

DÜZENLEME KURULU Kongre Başkanı Salih PEKMEZCİ Kongre Eş Başkanı Tayfun YÜCEL Genel Sekreter M. Mahir ÖZMEN Bilimsel Sekreterya Kaya SARIBEYOĞLU Hakan YANAR Üyeler Ediz ALTINLI Acar AREN Gürhan ÇELİK Cemalettin ERTEKIN Recep GÜLOĞLU Ahmet Nuray TURHAN



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